ABstracts -- SFB->Th17 - CPG Islands in PSOR STREAM - CCR6 - A20 - IL23 - Byron Links - Gut Microbes RISING? TLR2 or TLR* - Cardiation & Bugs - +++
randall
Hey.. i've got invisible psor plaques ALL over me now. LOL
Why?
I dunno... i thought it after reading this abstract:
http://www.ncbi.nlm.nih.gov/pubmed/21228808
J Invest Dermatol. 2011 Feb;131(2):283-5.
Gone but not forgotten: lesional memory in psoriatic skin.
Clark RA.
Harvard Skin Disease Research Center and Department of Dermatology,
Brigham and Women's Hospital, Boston, Massachusetts, USA.
Abstract
One of the most frustrating aspects of treating psoriasis is the
tendency of psoriatic skin lesions to recur after therapy has been
discontinued. Not only do lesions recur, but they often recur in the
same anatomical locations, expanding to the size they were before
therapy. This engenders feelings of frustration and futility in both
patients and the dermatologists who care for them. In this issue,
Suárez-Fariñas and colleagues identified a gene set-the residual
disease genomic profile-of psoriasis, suggesting the presence of both
immunologic and structural abnormalities within healed psoriatic
lesions. By understanding this ____"invisible lesion," _____we may be
one step closer to curing psoriasis.
PMID: 21228808
So i'm like 30-70% invisible pasi now? Leagues of invisible lesions?
Wow i hoPe the memory in my skin is GONE with the SFB i
knocked outa my guts with kimchi? LOL
How simPle is that?
WOW or HUGE comes to mind....
======================
Why don't they do a meta analysis on this GROUP instead?
What are you on about now?
Look at this gwas for psor snps and inflammatory pathways.
It's.... i'll let you tell me.
http://www.ncbi.nlm.nih.gov/pubmed/21226955
BMC Bioinformatics. 2011 Jan 12;12(1):17.
Pathway-based analysis using reduced gene subsets in genome-wide
association studies.
Zhao J, Gupta S, Seielstad M, Liu J, Thalamuthu A.
Abstract
ABSTRACT:
BACKGROUND: Single Nucleotide Polymorphism (SNP) analysis only
captures a small proportion of associated genetic variants in Genome-
Wide Association Studies (GWAS) partly due to small marginal effects.
Pathway level analysis incorporating prior biological information
offers another way to analyze GWAS's of complex diseases, and promises
to reveal the mechanisms leading to complex diseases. Biologically
defined pathways are typically comprised of numerous genes. If only a
subset of genes in the pathways is associated with disease then a
joint analysis including all individual genes would result in a loss
of power. To address this issue, we propose a pathway-based method
that allows us to test for joint effects by using a pre-selected gene
subset. In the proposed approach, each gene is considered as the basic
unit, which reduces the number of genetic variants considered and
hence reduces the degrees of freedom in the joint analysis. The
proposed approach also can be used to investigate the joint effect of
several genes in a candidate gene study.
RESULTS: We applied this new method to a published GWAS of psoriasis
and identified 6 biologically plausible pathways, after adjustment for
multiple testing. The pathways identified in our analysis overlap with
those reported in previous studies. Further, using simulations across
a range of gene numbers and effect sizes, we demonstrate that the
proposed approach enjoys higher power than several other approaches to
detect associated pathways.
CONCLUSIONS: The proposed method could increase the power to discover
susceptibility pathways and to identify associated genes using GWAS.
In our analysis of genome-wide psoriasis data, we have identified a
number of relevant pathways for psoriasis.
PMID: 21226955
____6 biologically plausible pathways____
Can you find the whole text and let me KNOW. LOL
------------
I'll give these guys a snip of my thinking.
It's SFB--->inducting excess---> TH17 with the usual genetic psor
suspects:
<but the negating effect of SFB-->Th17 on TREGs is critical>
And all psor susPects weigh in on these pathways right here:
<from current daily abstracts. w>
http://www.ncbi.nlm.nih.gov/pubmed/21226422
J UOEH. 2010 Dec 1;32(4):317-28.
Psoriasis and other Th17-mediated skin diseases.
Tokura Y, Mori T, Hino R.
Department of Dermatology, School of Medicine, University of
Occupational and Environmental Health, Japan.
Abstract
T helper (Th) 17 cells have crucial functions in host defense, and
dysregulated Th17 responses mediate a variety of autoimmune and
inflammatory conditions. Th17 cells coexpress interleukin (IL)-22, and
its receptor is expressed on epidermal keratinocytes. IL-17 and IL-22
cooperatively enhance some immunological responses. A close
relationship between IL-17 and the cutaneous milieu has been suggested
by a number of observations. IL-17 induces the production of certain
cytokines, chemokines and antimicrobial peptides by keratinocytes, and
its cooperation with IL-22 has been documented. Recent findings have
suggested that Th17 cells profoundly participate in the pathogenesis
of certain skin disorders, in particular, psoriasis. The concept of
the subsets of T cells responsible for psoriasis has been modified in
the order of Th1, T cytotoxic 1, and again Thl, and Thl7 cells. IL-22
is the strongest cytokine in the keratinocyte-proliferative ability.
Since IL-22 is produced by Th17 cells, they are crucial for the
proliferation of keratinocytes. Furthermore, IL-22 with the help of
IL-17 can induce the critical events of psoriasis, including signal
transducer and activator of transcription 3 (STAT3) activation,
cytokine/chemokine (IL-8 etc.) production, and antimicrobial peptide
elaboration. For maintaining Th17 cells, IL-23 is required and is
released from tumor necrosis factor-alpha (TNF-alpha) and inducible
nitric oxide synthetase (iNOS)-producing dendritic cells (TIP-DCs).
TIP-DCs are activated via an autocrine mechanism by virtue of TNF-
alpha. The above cytokine network in the pathogenesis of psoriasis has
been proven by the therapeutic effectiveness of cytokine-blocking
biologics. Antibodies against TNF-alpha or its soluble receptor have
already been widely used in the treatment of psoriasis. The
involvement of Th17 cells has also been shown in allergen-specific
immune responses. The percentage of Th17 cells is increased in the
peripheral blood of patients with atopic dermatitis (AD) and
associated with the severity of AD. Drug eruption is another disease
where Th17 cells are involved in the pathogenesis. The percentage of
circulating Th17 cells are increased in drug-induced hypersensitivity
syndrome, etc. Th17 cells and IL-22 are increased in patients with
acute generalized exanthematous pustulosis. Since IL-17 and IL-22
cooperatively stimulate keratinocytes to produce IL-8, keratinocyte-
derived IL-8 contributes to the accumulation ofneutrophils in the
lesional epidermis of this drug eruption.
PMID: 21226422
More Th17 and P please?
OK how about Th17 and PPP?
Love it.
http://www.ncbi.nlm.nih.gov/pubmed/21229362
Increased peripheral Th17 in patients with pustulosis palmaris et
plantaris.
[...] PMID: 21229362
Get some immune negating sunshine?
Right, those uvb's kick immunity southweird for sure:
http://www.ncbi.nlm.nih.gov/pubmed/21227895
Eur J Dermatol. 2011 Jan 13. [Epub ahead of print]
Systemic photochemotherapy decreases the expression of IFN-γ, IL-12p40
and IL-23p19 in psoriatic plaques.
[...] PMID: 21227895
The only problem with this is bcc and scc are some future point in
time. :(
------------
Is your PsA really RA or not?
http://www.ncbi.nlm.nih.gov/pubmed/21225692
Arthritis Rheum. 2011 Jan 10.
Characterization of CCL19 and CCL21 in rheumatoid arthritis.
Pickens SR, Chamberlain ND, Volin MV, Pope RM, Mandelin AM 2nd,
Shahrara S.
Department of Medicine, Feinberg School of Medicine, Northwestern
University Chicago, IL 60611.
Abstract
OBJECTIVE: The aim was to characterize the expression of CCL19 and
CCL21 in rheumatoid arthritis (RA) synovial tissue and to examine
their regulation and pathogenic role in macrophages and RA synovial
tissue fibroblasts.
METHODS: Expression of CCL19 and CCL21 was demonstrated in RA and
normal (NL) synovial tissues employing immunohistochemistry. CCL19 and
CCL21 levels were quantified in fluids from osteoarthritis (OA),
juvenile idiopathic arthritis (JIA), psoriatic arthritis (PsA) and RA
using ELISA. Regulation of CCL19 and CCL21 expression was determined
in RA peripheral blood in vitro differentiated macrophages as well as
RA synovial tissue fibroblasts by real-time RT-PCR. CCL19 and CCL21
activated peripheral blood in vitro differentiated macrophages and RA
synovial tissue fibroblasts were examined for proangiogenic factor
production employing ELISA.
RESULTS: CCL19 and CCL21 were elevated in RA synovial tissue compared
to NL controls. Levels of CCL19 and CCL21 were greatly increased in RA
and PsA synovial fluid versus OA synovial fluid. In RA macrophages and
fibroblasts, expression of CCL19 was increased by LPS, TNF-α and IL-1β
stimulation. However, CCL21 expression was modulated by IL-1β in RA
fibroblasts as well as TNF-α and RA synovial fluid in RA macrophages.
CCL19 and CCL21 activation induced VEGF and Ang-1 production from RA
synovial tissue fibroblasts and secretion of IL-8 and Ang-1 from
macrophages.
CONCLUSION: We identify, for the first time, regulators of CCL19 and
CCL21 in RA fibroblasts and RA peripheral blood in vitro
differentiated macrophages and we document a novel role of CCL19/21 in
RA angiogenesis.
PMID: 21225692
===============
OK so how do we do what WE need to do?
Either use epigenetic kung fu or epistatic Qi Gong?
Right... unPlug the myth e lations of our repitilian cpg islands. LOL
Huh?
Right huh....
Cpg and methylations an itch or bytch?
http://www.ncbi.nlm.nih.gov/pubmed/21228329
Blood. 2011 Jan 12.
Epigenetic modification of the human CCR6 gene is associated with
stable CCR6 expression in T cells.
Steinfelder S, Floess S, Engelbert D, Haeringer B, Baron U, Rivino L,
Steckel B, Gruetzkau A, Olek S, Geginat J, Huehn J, Hamann A.
Charite University Medicine Berlin, Research Centre for
ImmunoSciences, Berlin, Germany;
Abstract
CCR6 is a chemokine receptor expressed on Th17 cells and regulatory T
cells that is induced by T cell priming with certain cytokines, but
how its expression and stability is regulated at the molecular level
is largely unknown. Here, we identified and characterized a non-coding
region of the human CCR6 locus that displayed unmethylated CpG motifs
(Differentially-Methylated-Region, DMR) selectively in CCR6(+)
lymphocytes. CCR6 expression on circulating CD4(+) T cells was stable
upon cytokine-induced proliferation, but partially down-regulated upon
TCR stimulation. However, CCR6 down-regulation was mostly transient
and the DMR within the CCR6 locus remained demethylated. Notably, in
vitro induction of CCR6 expression with cytokines in TCR-activated
naive CD4(+) T cells was not associated with a demethylated DMR and
resulted in unstable CCR6 expression. Conversely, treatment with the
DNA methylation inhibitor 5'-azacytidine induced demethylation of the
DMR and led to increased and stable CCR6 expression. Finally, when
cloned into a reporter gene plasmid the DMR displayed transcriptional
activity in memory T cells that was suppressed by DNA methylation. In
summary, we have identified a non-coding region of the human CCR6 gene
with methylation-sensitive transcriptional activity in CCR6(+) T cells
that controls stable CCR6 expression via epigenetic mechanisms.
PMID: 21228329
----
22 hits: psoria* AND CCR6 - pubmed:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=psoria*+AND+ccr6
#4 in this search does RA and PsA with th17
http://www.ncbi.nlm.nih.gov/pubmed/20583102
Role of Th17 cells in human autoimmune arthritis.
Leipe J, Grunke M, Dechant C, Reindl C, Kerzendorf U, Schulze-Koops H,
Skapenko A.
Medizinische Poliklinik and University of Munich, Munich, Germany.
Abstract
OBJECTIVE: To delineate the role of Th17 cells in the pathogenesis of
autoimmune arthritides.
METHODS: Th17 cells were analyzed in well-defined homogeneous cohorts
of patients with the prototypical autoimmune arthritides rheumatoid
arthritis (RA) and psoriatic arthritis (PsA), grouped according to
patients who had very early active RA (n = 36; mean disease duration
2.8 months, Disease Activity Score in 28 joints 5.0) and those who had
very early active PsA (n = 20; mean disease duration 2.3 months), none
of whom had received treatment with glucocorticoids or disease-
modifying antirheumatic drugs, as well as patients with established RA
(n = 21; mean disease duration 68 months) who were considered either
responders or nonresponders to therapy. Groups of healthy individuals
and patients with osteoarthritis (a noninflammatory arthritis) were
used as control cohorts. Expression of T lineage-specific
transcription factors (RORC, T-bet, GATA-3, and FoxP3) and the
response of CD4 T cells to Th17 cell-inducing conditions were analyzed
in vitro.
RESULTS: The frequencies of Th17 cells and levels of interleukin-17
strongly correlated with systemic disease activity at both the onset
and the progression of RA or PsA. The values were reduced to control
levels in patients with treatment-controlled disease activity. Th17
cells were enriched in the joints, and increased frequencies of
synovial Th17 cells expressed CCR4 and CCR6, indicative of selective
migration of Th17 cells to the joints. The intrinsically elevated
expression of RORC, accompanied by biased Th17 cell development, and
the resistance of Th17 cells to a natural cytokine antagonist in
patients with RA and patients with PsA were suggestive of the
underlying molecular mechanisms of uncontrolled Th17 activity in these
patients.
CONCLUSION: Th17 cells play an important role in inflammation in human
autoimmune arthritides, both at the onset and in established disease.
PMID: 20583102
---
www.ncbi.nlm.nih.gov/pubmed/19662682
CCR6 is required for IL-23-induced psoriasis-like inflammation in
mice.
<snip>
---
http://en.wikipedia.org/wiki/C-C_chemokine_receptor_type_6
[...] Function
This protein belongs to family A of G protein-coupled receptor
superfamily. The gene is preferentially expressed by immature
dendritic cells and memory T cells. The ligand of this receptor is
macrophage inflammatory protein 3 alpha (MIP-3 alpha). This receptor
has been shown to be important for B-lineage maturation and antigen-
driven B-cell differentiation, and it may regulate the migration and
recruitment of dentritic and T cells during inflammatory and
immunological responses.
<snip>
Why do this again?
Your right, i'm gonna give you the links instead:
Goes to these two:
CCR6- LPS- TH17- IL-23- IL-22- Th9 -TGF-beta - CCR6 - AP-1 - JAK3:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_thread/thread/3316b383cafd49bf/ec7e76bc3ad46b64?hl=en&lnk=gst&q=ccr6+Th17+IL-23++TNF+lipopolysaccharide+(LPS)#ec7e76bc3ad46b64
& Tobacco to RAISE IL-10 & Th2-- Lower's Th17?
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_thread/thread/9ba56c3592ab42c8/eb5be4870aa78896?hl=en&lnk=gst&q=ccr6+Th17+IL-23++TNF+lipopolysaccharide+(LPS)#eb5be4870aa78896
Don't worry there are folks nearly as strange as i? LOL
OK so we have a base to work off of.
And?
Then cpg islands in the stream of inflammations.
Duh..
16 results for cpg islands -P NG: (13 of them have kicker term:
methylation)
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=cpg+islands&start=0&scoring=d&hl=en&
Let's find some terms for this?
How about [ cpg islands methylation reptile dna unmethylation ]?
Looks good to me.
And a little change:
http://www.google.com/search?hl=en&q=cpg+islands+methylation+reptile+dna+unmethylated&btnG=Search&aq=f&aqi=&aql=&oq=
http://www.biomedcentral.com/1471-2105/11/S7/S2
==============
Ok so that last one is a little deeP. LOL
------------
Making it more germane and less nebulous?
sure 12 hits : psoria* AND cpg - pubmed:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=psoria*+AND+cpg
#3 of this dozen:
http://www.ncbi.nlm.nih.gov/pubmed/19648272
J Immunol. 2009 Sep 1;183(5):3109-17. Epub 2009 Jul 31.
Requirement for DNA CpG content in TLR9-dependent dendritic cell
activation induced by DNA-containing immune complexes.
Yasuda K, Richez C, Uccellini MB, Richards RJ, Bonegio RG, Akira S,
Monestier M, Corley RB, Viglianti GA, Marshak-Rothstein A, Rifkin IR.
Department of Medicine, Boston University School of Medicine, Boston,
MA 02118, USA. kyasuda @bu.edu
Abstract
Although TLR9 was originally thought to specifically recognize
microbial DNA, it is now evident that mammalian DNA can be an
effective TLR9 ligand. However, the DNA sequence required for TLR9
activation is controversial, as studies have shown conflicting results
depending on the nature of the DNA backbone, the route of DNA uptake,
and the cell type being studied. In systemic lupus erythematosus, a
major route whereby DNA gains access to intracellular TLR9, and
thereby activates dendritic cells (DCs), is through uptake as a DNA-
containing immune complex. In this report, we used defined dsDNA
fragments with a natural (phosphodiester) backbone and show that
unmethylated CpG dinucleotides within dsDNA are required for murine DC
TLR9 activation induced by a DNA-containing immune complex. The
strongest activation is seen with dsDNA fragments containing optimal
CpG motifs (purine-purine-CpG-pyrimidine-pyrimidine) that are common
in microbial DNA but rare in mammalian DNA. Importantly, however,
activation can also be induced by CpG-rich DNA fragments that lack
these optimal CpG motifs and that we show are plentiful in CpG islands
within mammalian DNA. No activation is induced by DNA fragments
lacking CpG dinucleotides, although this CpG-free DNA can induce DC
activation if internalized by liposomal transfection instead of as an
immune complex. Overall, the data suggest that the release of CpG-rich
DNA from mammalian DNA may contribute to the pathogenesis of
autoimmune diseases such as systemic lupus erythematosus and psoriasis
in which activation of TLR9 in DCs by self DNA has been implicated in
disease pathogenesis.
PMID: 19648272
PMCID: PMC2860771
Free PMC Article <see above link for links>
--------------
Should i do cpg's versus SFB and Th17?
No... let's do MOM is full of craP?
What? Shut your mouth... mo fo...
Hey nothing personal here:
Check it:
http://www.sfgate.com/cgi-bin/article.cgi?f=/c/a/2011/01/14/MNN41GL1NQ.DTL&tsp=1
[...] The study, which was funded by the Pew Charitable Trusts and a
grant from the Passport Science Innovation Fund, analyzed data from
the pregnant women provided by the 2003-04 National Health and
Nutritional Examination Survey, a nationally representative sample of
the U.S. population.
The chemicals found in 99 percent to 100 percent of the women included
certain PCBs, organochlorine pesticides, perfluorinated compounds,
phenols, PBDEs, phthalates, polycyclic aromatic hydrocarbons and
perchlorate.
<snip>
Wow bad stuff huh? LOL
Let's exhume Jeanne Calment and see if her tissues have these?
Right, she only lived for 122 and a half years.
Can your liver tolerate it like her's did?
More olive oil (n9's) and port wine and cig's i guess?
Maybe not the whacky tobacco unless it's high IL-10?
Right inside joke. <snort>
-----------
Back to the grind:
34 hits - cpg unmethylated autoimmun* - pubmed:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=cpg+unmethylated+autoimmun*
Wow, the first one with japanese guys who think likeeee ME?
Must be the implant of japanese sourced human microbes i got in 1999.
LOL
I'm turning in to them .. (<w> <G>)
http://www.ncbi.nlm.nih.gov/pubmed/21191889
Eur J Immunol. 2010 Dec 1.
5'-Phosphate oligodeoxynucleotides enhance the phosphodiester-CpG DNA-
induced inflammatory response in macrophages.
Yoshida H, Nishikawa M, Kiyota T, Uno S, Toyota H, Takahashi R, Narita
M, Takakura Y.
Department of Biopharmaceutics and Drug Metabolism, Graduate School of
Pharmaceutical Sciences, Kyoto University, Kyoto, Japan.
Abstract
Dying cells release genomic DNA into the surroundings where the DNA is
first degraded to oligodeoxynucleotides, then to nucleotides,
nucleosides and so on. Given that the unmethylated CpG dinucleotide
(CpG motif), which is characteristic of bacterial DNA, is also
contained in mammalian DNA and has been reported to be involved in the
exacerbation of DNA-associated autoimmune diseases, we investigated
whether nucleotides and nucleosides affect immune responses to
phosphodiester (PO)-CpG DNA. Addition of non-CpG DNA to RAW264.7,
murine macrophage-like cells, induced no significant TNF-α production
irrespective of treatment with DNase I; however, DNase I-treated, but
not untreated, non-CpG DNA increased the PO-CpG DNA-mediated TNF-α
production. This increase was not observed with phosphorothioate-CpG
DNA or ligands for TLR3, TLR4 or TLR7. Deoxynucleotides with a 5'-
phosphate showed similar effects to those of DNase I-treated non-CpG
DNA, but DNase II-treated DNA or deoxynucleosides did not.
Subcutaneous injection of PO-CpG DNA into the mouse footpad induced
little swelling of the paw; however, significant swelling was observed
when DNase I-treated DNA was co-injected with PO-CpG DNA. These
results imply that PO-CpG DNA-dependent inflammatory responses are
increased by DNA molecules with a 5'-phosphate; such molecules could
therefore be considered as exacerbating factors for CpG motif-related
inflammation.
PMID: 21191889
Let's see now:
Only 10 hits with no UN on methylated for the last search:
10 hits: cpg methylated autoimmun* - pubmed:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=cpg+methylated+autoimmun*
If you don't see this your surely not gonna get SFB ramifications.
Segmented filamentous bacteria or bacterium induct Th17 cells.
That and LPS and TLR's can fire up a host of problems for
autoimmunity.
But for me SFB is KEY.
Rest time?
Rest your mind?
OK...
Fun stuff?
OK
Liver Cells with your heart in MIND?
Will knock out or take out the craP in MOM?
I hoPe...
http://www.wellnessresources.com/health/articles/a_surprise_finding_endothelial_cells_rejuvenate_your_liver/
A Surprise Finding: Endothelial Cells Rejuvenate Your Liver
Thursday, January 13, 2011 - Byron Richards, CCN
Your liver is the “brain of your body” and its healthy function is
required for your ongoing well being. Your liver is potentially
damaged by pollution, excess alcohol, medications, street drugs,
internal “plumbing” problems, and excess food. For the first time, a
process by which your liver can regenerate itself has been
identified. As it turns out the endothelial cells1 lining the
circulatory system within your liver orchestrate the rejuvenation
process.
This is the first time scientists have ever documented a specific
mechanism involved with liver rejuvenation. They hope to use the
information to help individuals with liver injury or diseased livers.
I think their discovery has immediate practical application value for
you in terms of maintaining optimal liver function and health.
Endothelial cells are the weak link in the circulatory system. They
form a thin layer, only one cell thick, which lines the insides of
your arteries. They are crucial regulators of nutrient uptake from
your circulation and instrumental in blood pressure regulation. When
they are injured, the plaquing process is set in motion and increases
potential for cardiovascular disease. In this context, the importance
of endothelial cells has been understood for quite some time.
This new study proves that endothelial cells within your liver secrete
signals that initiate and sustain the rejuvenation of your liver.
They enable stem cells to form new liver cells and then coordinate the
linking together of the liver cells to form new organ structure.
The problem is that endothelial cells are in contact with the contents
of the blood. The greater the number of stress chemicals, toxins,
pollutants, antigens, junk food, and other irritants that come into
contact with them, the greater the potential to damage these cells.
This means that their ability to orchestrate rejuvenation would be
compromised.
Furthermore, injured endothelial cells cannot be replaced by those
next to them splitting and dividing so as to form a new layer.
Rather, new endothelial cells must be produced in the bone marrow and
travel to the liver (or anywhere else in the circulation) in order to
fix the injured area. This means bone health must be maintained in
order to have a supply of rejuvenating endothelial cells. This may be
one key reason that bone health is associated with longevity
(independent of the fracture issue).
The researchers also demonstrated that this mechanism of liver organ
rejuvenation likely applies to all organs, although endothelial cell
growth factors for each organ likely have different signals and these
have not yet been figured out. However, the concept of preserving the
health of your endothelial cells so as to aid general organ
rejuvenation seems to be an emerging new fundamental principle of
health.
In addition to bone health, this places a new emphasis on keeping your
blood “cleaner” and your endothelial cells protected. This means the
entire subject of detoxification is of immense importance. Nutrients
that preserve the lining of the insides of your arteries including
your endothelial cells. Top choices would include DHA, tocotrienol E,
silymarin, taurine, and grape seed extract. However, there are many
nutrients likely to help in one way or another.
The take home message is that you are more likely to be able to
naturally rejuvenate your body organs (i.e., live longer and
healthier) with cleaner blood, nourished endothelial cells lining
your blood stream, and good bone health.
--------
OK GOOD even with all that techno crap in us we can DETOX...
Good, good, goo, go goo brains. LOL
WhooPs just had a dementia moment...
Odd?
Not really... i pink to mush at times...< gork?>
-------------
Quickly go outside and get some sunshine and exercise...
Yep... but will it help to dexoT?
http://www.wellnessresources.com/health/articles/walking_speed_predicts_longevity/
Walking Speed Predicts Longevity
Tuesday, January 11, 2011 - Byron Richards, CCN
The Journal of the American Medical Association1 began the New Year on
the right foot – which was quickly followed by the left foot – your
ability to maintain a brisk walking pace as you age directly predicts
longevity.
For example, if you are 75 and maintain a walking pace of 3 miles per
hour you are likely to live at least 7 more years if you are a man and
18 more years if you are a woman. The researchers found a
statistically significant increased lifespan based on walking speed in
9 studies that were evaluated.
I might point out that no such claim can be made for drugs or any
combination of drugs. If older Americans stuck with a good diet,
regular exercise, and other natural health strategies they would fair
far better than the Big Pharma model of progressive drug poisoning
during aging.
<snip>
Omg, omg i'm gonna get some chromium or lick it off my bumPer?
http://www.wellnessresources.com/health/articles/chromium_improves_cognitive_function_in_older_adults/
Chromium Improves Cognitive Function in Older Adults
Wednesday, January 12, 2011 - Byron Richards, CCN
In a placebo-controlled, double-blind trial, older adults with
cognitive decline were supplemented with chromium picolinate1 for 12
weeks. Several parameters of brain function improved, and brain
imaging showed a number of brain regions to be more active.
Chromium is known to help blood sugar transport into cells more
efficiently and many studies show that it can help to overcome the
problem of insulin resistance. Your brain needs a consistent supply
of blood sugar (fuel) in order to make energy to function. This study
shows that impaired brain function is at least partly involved with
insulin resistance in the brain.
Simple basics should never be ignored when trying to overcome any
health problem, including cognitive decline. Exercise helps pump
blood to your head, following the Leptin Diet helps sugar enter your
brain in a better way, and blood sugar support nutrients like chromium
help to overcome age-associated insulin resistance in the brain.
<snip>
http://www.wellnessresources.com/health/articles/breastfeeding_boosts_future_muscle_strength_of_child/
Breastfeeding Boosts Future Muscle Strength of Child
======================
http://www.eurekalert.org/pub_releases/2011-01/foas-tmi011311.php
The microbes in our gut regulate genes that control obesity and
inflammation
New research in the FASEB Journal suggests that the absence of
intestinal toll-like receptor 2 affects gut bacteria, pointing to a
new way to manage weight and intestinal problems
If you are looking to lose weight in the coming year, you may need
help from an unexpected place: the bacteria in your gut. That's
because scientists have discovered that the bacteria living in your
intestines may play a far more significant role in weight loss and
gastrointestinal problems than ever imagined. In a new research report
published online in The FASEB Journal (http://www.fasebj.org),
researchers show that a deficiency of Toll-like receptor 2 (Tlr2)—used
by mammals (including humans) to recognize resident microbes in the
intestines—leads to changes in gut bacteria that resemble those of
lean animals and humans. This discovery builds on previous research
demonstrating that a deficiency of TLR2 protects against obesity,
while at the same time promoting gastrointestinal problems like
excessive inflammation. It also shows that genes controlling TLR2
expression play a very important role in one's gastrointestinal health
and weight management.
"Our work highlights the remarkable capacity for an orchestrated
reprogramming of the intestinal inflammatory network to overcome
significant genetic challenges in the mammalian bowel," said Richard
Kellermayer, Ph.D., a researcher involved in the work from the Section
of Pediatric Gastroenterology, Hepatology and Nutrition at Baylor
College of Medicine in Houston. "The appropriate exploitation of this
remarkable capacity may provide means for the prevention and optimized
treatment of common metabolic (such as obesity and diabetes) and
gastrointestinal disorders."
To make this discovery, Kellermayer and colleagues studied normal mice
and mice deficient in TLR2 using the large intestinal lining of these
mice. They compared the TLR2-deficient ones to the normal group, as
well as the bacteria, the epigenome (more specifically DNA
methylation, a molecular change in the DNA associated with decreased
gene expression), and the gene expression of the animals. The
researchers found that the absence of TLR2 leads to microbial changes
in the gut that resemble lean animals and humans, as well as
immunologic changes similar to those observed in ulcerative colitis.
"Every New Year, a significant percentage of us resolve ourselves to
lose weight," said Gerald Weissmann, M.D., Editor-in-Chief of The
FASEB Journal, "but national statistics on obesity show that we're
failing fast. This research linking gut bacteria to TLR2 expression
opens entirely new doors for weight control solutions, first by
cementing TLR2 as a drug target for obesity, and second by providing
further evidence that managing gut bacteria may be an important and
effective way to control weight. The challenge, of course, is to find
a way to tip the scales just enough to keep weight under control
without causing serious gastrointestinal problems."
###
The FASEB Journal (http://www.fasebj.org) is published by the
Federation of the American Societies for Experimental Biology (FASEB)
and celebrates its 25th anniversary in 2011. Over the past quarter
century, the journal has been recognized by the Special Libraries
Association as one of the top 100 most influential biomedical journals
of the past century and is the most cited biology journal worldwide
according to the Institute for Scientific Information.
FASEB comprises 23 societies with more than 100,000 members, making it
the largest coalition of biomedical research associations in the
United States. FASEB enhances the ability of scientists and engineers
to improve—through their research—the health, well-being and
productivity of all people. FASEB's mission is to advance health and
welfare by promoting progress and education in biological and
biomedical sciences through service to our member societies and
collaborative advocacy.
Source: Richard Kellermayer, Scot E. Dowd, R. Alan Harris, Alfred
Balasa, Tiffany D. Schaible, Randy D. Wolcott, Nina Tatevian, Reka
Szigeti, Zhijie Li, James Versalovic, and C. Wayne Smith
Colonic mucosal DNA methylation, immune response, and microbiome
patterns in Toll-like receptor 2-knockout mice. FASEB J; doi:10.1096/
fj.10-172205 ; http://www.fasebj.org/content/early/2011/01/11/fj.10-172205.abstract
-----
Abstract
The connection between intestinal microbiota and host physiology is
increasingly becoming recognized. The details of this dynamic
interaction, however, remain to be explored. Toll-like receptor 2
(Tlr2) is important for its role in bacterial recognition, intestinal
inflammation, and obesity-related metabolic changes. Therefore, we
sought to determine the epigenomic and metagenomic consequences of
Tlr2 deficiency in the colonic mucosa of mice to gain insights into
biological pathways that shape the interface between the gut
microbiota and the mammalian host. Colonic mucosa from wild type (WT)
and Tlr2−/− C57BL/6 mice was interrogated by microarrays specific for
DNA methylation and gene expression. The mucosal microbiome was
studied by next-generation pyrosequencing of bacterial 16S rRNA. The
expression of genes involved in immune processes was significantly
modified by the absence of Tlr2, a number of which correlated with DNA
methylation changes. The epigenomic and transcriptomic modifications
associated with alteration in mucosal microbial composition. Several
bacterial species, including members of the Firmicutes were
significantly different in abundance between WT and Tlr2−/− animals.
This manuscript highlights the intimate interrelationships between
expression of immune-related genes and immunity pathways in the host
with compositional and functional differences of the mammalian
microbiome.—
48- "Kellermayer R"[Author] - pubmed:
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Kellermayer%20R%22%5BAuthor%5D
---------
http://www.medicalnewstoday.com/articles/212763.php
Accurate Interpretation Of Antinuclear Antibodies Test Key To
Confirming Autoimmune Disease
The presence of antinuclear antibodies (ANA) indicates the possibility
of autoimmunity and the indirect immunofluorescence (IIF) assay on
HEp-2 cells is the standard blood test (ANA-HEp-2) used to detect ANA.
However, studies have shown that a "false-positive" ANA test occurs in
up to 13% of healthy individuals. In such cases the test detects the
presence of autoantibodies that apparently are not associated with
autoimmunity. Researchers from Brazil have now uncovered
distinguishing characteristics of the ANA test in healthy individuals
and patients with autoimmune disease, reducing the likelihood of an
erroneous autoimmune disorder diagnosis. Their findings are published
in the January 2011 issue of Arthritis & Rheumatism, a journal of the
American College of Rheumatology (ACR).
The immune system is responsible for protecting the body against
foreign invaders and infection, but in some individuals the immune
system repeatedly attacks healthy cells in the body resulting in an
autoimmune disease. According to the Centers for Disease Control and
Prevention (CDC) autoimmune diseases which include rheumatoid
arthritis, Sjögren's syndrome, and systemic lupus erythematosus affect
up to 8% (22 million individuals) of the U.S. population.
The Brazilian research team, led by Luis Andrade, MD, PhD, from the
Federal University of São Paulo, recruited 918 healthy individuals
(634 females and 284 males) between the ages of 18 and 66 years for
this study. In the control group were 153 patients with autoimmune
rheumatic diseases that included lupus (87), systemic sclerosis (45),
Sjögren's syndrome (11) and idiopathic inflammatory myopathy (10). To
determine the concentration of ANA in the blood, ANA-HEp-2 tests were
run on all participants and considered positive if a well defined IIF
pattern was identified.
"The ANA-HEp-2 test is positive in a sizable portion of the general
population and our findings established distinguishing characteristics
between healthy individuals and patients with autoimmune disease which
is essential to accurately interpret the test results," explained Dr.
Andrade. Researchers determined that positive ANA-HEp-2 tests in
healthy participants occurred predominantly as a nuclear fine speckled
(NFS) pattern (at low to moderate titer) or as a nuclear dense fine
speckled (NDFS) pattern (frequently at high titer) in 46% and 33% of
ANA-positive healthy individuals, respectively. Healthy participants
did not present a nuclear coarse speckled (NCS) or a nuclear
homogeneous (Ho) pattern.
In those with autoimmune disease the ANA-HEp-2 showed positive results
at a predominantly moderate to high titer. A distinct ANA-HEp-2
pattern profile was observed, characterized by the absence of the NDFS
pattern and the exclusive occurrence of the NCS (26%), centromeric
(8%), nuclear homogeneous (7%), and cytoplasmic dense fine speckled
(3%) patterns. ANA-positive patients with confirmed autoimmune
diseases also showed the presence of the NFS (42%), but at a higher
titer than in healthy individuals.
At the end of a 4-year follow-up period 73% of the ANA-positive
healthy individuals retained a positive test result, but did not
develop any symptoms of autoimmune rheumatic disease. "Our study
confirms that the ANA-HEp-2 pattern is critical in properly diagnosing
autoimmune disorders and future research should attempt to reproduce
the interpretation of test results among different ANA experts and ANA-
HEp-2 slides brands," Dr. Andrade concluded.
<snip>
------------
http://www.medicalnewstoday.com/articles/212957.php
[...] In the paper, researchers describe processing the tissue using
cell cultures and genomic analysis to look for the presence of
culturable bacteria. In addition, they looked at five pairs of
diseased and healthy arterial tissue. The use of cell cultures aided
in the isolation of the bacillus Enterobacter hormaechei from the
patient's tissue. Implicated in bloodstream infections and other life-
threatening conditions, the isolated bacteria were resistant to
multiple antibiotics. Surprisingly, using quantitative methods, this
microbe was further identified in very high numbers in diseased but
not in healthy arterial tissues.
The data suggest that a chronic infection may underlie the process of
atherosclerosis, an infection that can be initiated by the systemic
dissemination of bacteria though different "gates" in the vascular
wall - as in the case of a septic patient, through intestinal
infection. The data support Dr. Kozarov's previous studies, where his
team identified periodontal bacteria in carotid artery, thus pointing
to tissue-destructing periodontal infections as one possible gate to
the circulation.
<snip>
http://www.medicalnewstoday.com/articles/151444.php
What Is A Heart Attack? What Causes A Heart Attack?
If the heart muscle does not have enough blood (and consequently
oxygen) it dies and a heart attack occurs. Another name for a heart
attack is myocardial infarction, cardiac infarction and coronary
thrombosis. According to Medilexicon's medical dictionary, a heart
attack is "infarction of a segment of heart muscle, usually due to
occlusion of a coronary artery". (Infarction = the process whereby an
area of dead tissue is caused by a loss of blood supply).
A heart attack usually happens when a blood clot develops in one of
the blood vessels that lead to the heart muscle (coronary arteries).
The clot, if it is big enough, can stop the supply of blood to the
heart. Blood supply to the heart can also be undermined if the artery
suddenly narrows, as in a spasm.
What are the symptoms of a heart attack?
Chest discomfort, mild pain
Coughing
Crushing chest pain
Dizziness
Dyspnea (shortness of breath)
Face seems gray
A feeling of terror that your life is coming to its end
Feeling really awful (general feeling)
Nausea
Restlessness
The person is clammy and sweaty
Vomiting
If you experience these symptoms, or witness another person with them,
call the emergency services immediately. In the United Kingdom the
telephone number is 999, in the USA and Canada it is 911, Australia
000, and New Zealand 111. Many cell phones' emergency number is 112.
<snip over 80% of this article - it's huge>
http://www.medicalnewstoday.com/articles/212954.php
Cardiologists Uncover New Heart Attack Warning Sign
[...] heart attack patients had elevated levels of the protein
fragment known as Caspase-3 p17 in their blood.
"We've discovered a new biomarker for heart attack, and showed that
apoptosis, or a particular kind of cell death, is a cause of heart
muscle damage." Liang says. "The ability to see a heart attack coming
with a simple blood test and to develop new therapies to block
apoptosis would enable us to get a head start on treatment and
preserve crucial heart muscle and cardiac function."
If it is successfully applied one day, researchers say the discovery
would mean another way to diagnose heart attack and the possible
development of new treatment.
<snip>
A person who is having a heart attack usually feels the pain in his/
her chest first. This pain then spreads to the neck, jaw, ears, arms,
and wrists. With some patients, the pain also makes its way into the
shoulder blades, the back, and the abdomen.
<snip>
======================
Wow this is great... I wished they started doing it YEARs ago... then
we'd KNOW more ON these toPics. <G>
http://www.eurekalert.org/pub_releases/2011-01/uoc--ssg011311.php
Scientists sequence gut microbes of premature infant
Cataloguing microbes in gut could lead to cause of necrotizing
enterocolitis
Scientists have for the first time sequenced and reconstructed the
genomes of most of the microbes in the gut of a premature newborn and
documented how the microbe populations changed over time.
Further studies involving more infants could eventually help
researchers understand the causes of various intestinal problems that
afflict preemies, in particular the sometimes fatal necrotizing
enterocolitis, according to researchers at the University of
California, Berkeley, the University of Pittsburgh School of Medicine
and Stanford University. One unresolved question is whether these
illnesses are caused by pathogenic strains of bacteria or just an
imbalance in the microbe populations in the gut.
The study was posted online Dec. 29 in advance of print publication in
the journal Proceedings of the National Academy of Sciences.
While this is not the first time that microbes in the human intestinal
tract have been sequenced as a community, this is the first
comprehensive look at a time series documenting colonization of the
gut of a premature newborn, and one of few completely assembled
community genomic datasets, said Jill Banfield, a UC Berkeley
professor of earth and planetary science and of environmental science,
policy and management.
"Sequencing of microbial communities has become exceedingly common,
but many researchers work with essentially unassembled data and often
analyze very short contiguous DNA sequences – genome fragments," she
said. "We actually go in and work out where the assemblies failed and
fix them – what's called curating the data – so we can build very
complete genomes for most of the microbes."
Pediatric surgeon Michael J. Morowitz, until recently at The
University of Chicago Medical Center but now with Children's Hospital
of Pittsburgh of the University of Pittsburgh Medical Center and an
assistant professor of surgery at the University of Pittsburgh School
of Medicine, first approached Banfield because of her pioneering work
over the past decade sequencing microbial communities in extreme
environments, such as the acid drainage from underground mines. He
suggested that she tackle a unique human environment, the newborn
intestinal tract. Unlike the adult gut, which may contain a couple of
thousand microbial species, the newborn's intestinal tract may be
colonized by only a handful, making it feasible to sequence the entire
community.
His interest stemmed from work with premature infants, most of whom
spend anywhere from two weeks to six months in the intensive care unit
before they're deemed healthy enough to go home. Between 5 and 10
percent of these preemies develop symptoms of necrotizing
enterocolitis (NEC), which requires rounds of antibiotics to halt, and
perhaps a third of these babies eventually require surgery to remove
parts of their intestines that have died.
"The actual impact of necrotizing enterocolitis in the ICU is even
larger, because feeding routines and other care are conducted around a
fear of NEC developing," Morowitz said.
Previous studies, however, have produced conflicting results about
NEC's cause. Some have found pathogenic bacteria associated with NEC,
while others have found no difference between the bacteria in babies
with and without NEC. Banfield, Morowitz and their collaborators
suspect that these results reflect the fact that researchers have
looked broadly at species or families of bacteria in the gut, rather
than at variants or strains. Although coexisting strains may have
genes that are 99 percent identical, their genomes could be
sufficiently distinct to make one bad and the other good.
"We already know that just a few genes can make one strain a pathogen
and one beneficial or commensal," meaning that the microbes live
amicably with their host, Banfield said. "We expect that a lot of the
issues with the colonization process in the gut that leads to disease
may be tracked to subtle differences in strains," she said. "So one
question on the table is, 'Are these very closely related strains
physiologically distinct, and in what ways'?"
The only way to get at these differences, she said, is to sequence the
entire genomes of the intestinal microbiota – not merely DNA fragments
or short DNA tags, which can be used to identify the genus or even
species of a microbe, but not the specific strain.
"Although a primary target of our research is NEC, it's become very
apparent that there are some fundamental unanswered questions just
about the colonization process under normal circumstances," Morowitz
added. "It's really important to get a handle on what the normal
process is first, and then, eventually, we can look closely at babies
with NEC and see if they deviate from what appears to be the normal
colonization process."
Other human diseases, including asthma, diabetes and obesity, have
been linked to problems with microbial colonization of the gut, and
several papers have reported symptomatic improvement after
"transplanting" fecal material from healthy individuals to patients
with a range of intestinal disorders.
Banfield, Morowitz and their colleagues followed a single premature
infant that had been delivered by cesarean and identified three
distinct communities of intestinal microbes present at different times
during the first month of the infant's life. The microbe populations
in these communities seemed to change after alterations in medication
and feeding, Morowitz said. Although it was presumably sterile at
birth, the infant's gut was quickly colonized by a set of known
intestinal microbes – bacteria and Archaea, primarily, but also
viruses, bacterial viruses (phage) and the naked lengths of DNA called
plasmids. When the baby went off antibiotics and switched from breast
feeding to intravenous feeding, the microbe populations completely
changed, with minor microbial members suddenly dominating and dominant
members declining.
Vincent Denef, a post-doctoral researcher in Banfield's lab who
contributed to the study, noted that such real-time studies are
powerful because "very rarely do we have the opportunity to observe
the dynamics of a naturally occurring system, such as the infant GI
tract, as it is transformed from sterile to functionally diverse."
The populations again shifted when intravenous feeding was replaced by
formula. Morowitz stopped collecting feces from dirty diapers after 21
days, and the infant was sent home healthy after 9 weeks in the ICU.
Though fecal samples were taken nearly every day, a complete genome
analysis was performed only for samples collected on days 10, 16, 18
and 21. For the other days, the microbial community was estimated
based on DNA tags (16S rRNA) that identify microbe families and
species, but not specific strains.
What surprised the researchers is that the microbial population was
comprised of members of at least 20 groups, many of which include
harmful as well as benign organisms. These included Staphylococcus, a
frequent cause of hospital infections; Pseudomonas, "the cause of an
enormous amount of morbidity in ICU patients, both children and
adults," Morowitz said; Serratia, a common cause of sepsis in general;
and Citrobacter, which can cause meningitis in babies. Yet, the baby
in this study appeared healthy throughout.
"The gut populations are highly dynamic, with large shifts through
three stages over time, but we saw an overabundance of gram-negative
organisms that we often associate with disease," he said.
"Particularly striking was the dominance of Pseudomonas for several
days, though the infant was clinically stable."
The seeming contradiction of a healthy infant with disease-causing
bacteria in her gut could be explained if the strains in the infant's
gut were benign, or if the balance of other microbes prevented
pathogenic microbes from causing problems.
Citrobacter, for example, is one type of bacteria that is reportedly
associated with NEC: one study found Citrobacter in three of four
infants with NEC, but in no control infants. Yet, in the current
study, sequencing of the gut microbiome on days 16, 18 and 21 revealed
the presence of two strains of Citrobacter, which fluctuated
significantly in proportions on the three days. "Those big shifts
could potentially have been very important for the medical state of
that baby," Banfield said. "Fortunately, the baby was fine."
The researchers found that those two strains were 99 percent similar
over areas of the genome that could be compared.
"Of particular interest were hot spots of rapid DNA evolution within
and between genes. Those potentially could be very important and
interesting," she said. "Though the two Citrobacter genotypes are
very, very similar over most of the genome, the results suggest that
they could be functioning in different ways because their genomes are
regulated differently."
Banfield noted that the intestinal community of the infant no doubt
would continue to shift repeatedly for a year or more after birth, as
the child encounters new microbes – courtesy of family, friends and
pets. These populations shift with the influx of new strains and
species and potentially because the resident microbes themselves
evolve by picking up new traits from the plasmids and phages living
alongside them.
"This is an ecological study," she emphasized. "One of the things we
are trying to do is bring into the field of medicine a high
resolution, ecological approach."
###
Other coauthors of the study are Brian C. Thomas of UC Berkeley,
Valeriy Poroykoa of the University of Chicago Pritzker School of
Medicine, and David A. Relman and Elizabeth K. Costello of the
Stanford University School of Medicine.
<snip>
----------------
Hot off the Montana grill... no time to vet but i've got to hit the
RAYs of UVB outside and xxercise now.
An innate immune source of IL-22:
NK-22 cells a subset of nK cells that are programmed to secrete
Il‑22 was recently discovered in the mucosa‑associated lymphoid
tissue (Malt)
of mice and humans.
These NK cells, known as NK‑22s, are specifically activated by Il‑23
to secrete Il‑22, which belongs to the family of Il‑10‑related
cytokines*
and has been proposed to have diverse roles in host defence and
disease pathogenesis, and has both pro‑inflammatory and
anti‑inflammatory effects
Importantly, Il‑22 in the gut and other mucosal surfaces seems to
protect the epithelial cell barrier between host and pathogen.
In humans, NK‑22s were identified in an nKp44+ subset of cD56+cD3–
nK cells found predominantly in the mucosal areas
of the tonsil and the ileal peyer’s patches....
*{10 x 2 (=20)+ 2,2,2 (22, 24, 26) & insert 19}
NK-22 cells and mucosal immunity
NK-22 cells rapidly produce Il-22 after being activated by il-23 and
are probably important for mucosal homeostasis and the protection
of mucosal sites during infection and inflammation.
The Il-22 receptor is expressed on several types of epithelial tissue—
particularly that of the skin and gastrointestinal tract (Wolk et al,
2004)
—rather than on immune cells.
Il-22 is thought to protect and maintain epithelial barriers through
the upregulation of anti-apoptotic molecules and bactericidal
proteins.
Indeed, NK-22 cell-conditioned media induces colon epithelial cell
proliferation, the activation of anti-apoptotic pathways and
the secretion of Il-10, which is an anti-inflammatory cytokine that is
important for the protection of mucosal cells (cella et al, 2009).
Early host defence against infection of the gastrointestinal tract by
Citrobacter (C.) rodentium has been shown to depend on Il-22
(zheng et al, 2008) and NK-22 cells appear in the small intestine
lamina propria after mice are infected with C. rodentium (cella et
al,
2009).Furthermore, the depletion of NK cells from C. rodentium-
infected Rag2–/– mice—which lack T-cell-produced Il-22—resulted
in accelerated mortality, suggesting a protective role for NK-22s in
this Il-22-dependent infection (Satoh-takayama et al, 2008; cella
et al, 2009).
Il-22 has also been shown to be protective against inflammatory
diseases, including hepatitis, autoimmune myocarditis
and inflammatory bowel disease.
A recent study in Rag1–/– mice demonstrated that nK cells can serve as
a source of protective il-22 in two murine models of inflammatory
bowel
disease (zenewicz et al, 2008). collectively, these studies suggest
that after an inflammatory response is elicited at mucosal barriers
and il-23 is produced by resident antigen-presenting cells,
NK-22s might provide an innate immune source of Il-22 that can help
to protect the host mucosa and control inflammation (Fig 3).
Il-22 promotes host defences in many cases, but it is also thought to
be involved in the pathogenesis of some diseases including psoriasis
and multiple sclerosis.
The primary adaptive immune source of Il-22 is Th-17 cD4+ t cells,
which also produce Il-17—a cytokine associated with
autoimmune disease pathogenesis—and are thought to have a pathogenic
role in the same diseases.
In contrast to tH17 cells, Malt-associated NK-22 cells specialize in
Il-22 production and do not produce Il-17 (cella et al, 2009).
Whether NK-22s mediate inflammatory diseases is
not yet known, although their lack of Il-17 suggests that this NK cell
subset
has the potential to exert protective Il-22-
mediated effects at mucosal sites without eliciting Th17-associated
pathology.
If this is the case, the dual role of il-22 as being both protective
and detrimental to the host would be explained by the cellular source
of Il-22 and the local cytokine milieu
================
randall doing what's next xxxercise.... and cardio work and D3 to the
MAX via RAH rah ra r...