Unutmaz - Treg's -- Foxp3 -- Runx - Rudensky- GARP- Bowcock- Git - Lamina Propria - Th17- Lacti Plantarum
randall
That last post for Th22 inspired this one.
How do we put the Th22 SUBSET to SLEEP?
Easy hit the sleep button?
Only if....
That button is REAL but how does it turn ON?
This button is IL-10 loaded.
And from my perspective you have to learn the sweet whey of randall...
I see the world from the yin yang OUT as
psoriasis is an iNSIDE OUT disease.
You can't TELL me that IL-10 and the lamina propria aren't the HOT
ZONE of Ai.
What else can keep inflammation fires burning for YEARs?
I suPPose you can try exPlaining Ai (autoimmune), but Dr. Unutmaz is
saying something right now.
I love Unutmaz btw. He's dialed in immunologically BIG TIME. Like
Littman on SFB's .... i hoPe. <g>
www.ncbi.nlm.nih.gov/pubmed/19841645
The gut feeling of Treg cells: IL-10 is the silver lining during
colitis.
__Unutmaz D__, Pulendran B.
Comment on:
Nat Immunol. 2009 Nov;10(11):1178-84.
Regulatory T cells (Treg's) that express the transcription factor
Foxp3 are pivotal in suppressing autoimmune responses. A report in
this issue describes a key role for interleukin 10 produced by lamina
propria macrophages in maintaining Foxp3 expression during
inflammatory responses in the intestine.
PMID: 19841645
http://en.wikipedia.org/wiki/FOXP3
Foxp3 is master regulator of Treg's
OK, ok, so we KNOW the Ai hot zone is Th17 dominated in the ileum from
SFB's ...
Or so Dan Littman and i think NOW.
What does unutmaz have to say about that?
Darn nutz, wish i had his cell phone number? <G>
Shall i look for CLUEs?
CaPitol idea...
How do some nice mice get fatal intestinal inflammation?
Easy..
**Treg-specific ablation of Stat3, a TF critical for TH17
differentiation**
www.ncbi.nlm.nih.gov/pubmed/19797626
CD4+ Regulatory T Cells Control TH17 Responses in a Stat3-Dependent
Manner.
Chaudhry A, Rudra D, Treuting P, Samstein RM, Liang Y, Kas A,
__Rudensky AY.___
Howard Hughes Medical Institute and Immunology Program, Memorial Sloan-
Kettering Cancer Center, New York, NY 10065, USA.; Department of
Immunology, University of Washington, Seattle, WA 98195, USA.
Distinct classes of protective immunity are guided by activation of
STAT transcription factor (TF) family members in response to
environmental cues. CD4(+) regulatory T cells (Tregs) suppress
excessive immune responses, and their deficiency results in a lethal,
multi-organ autoimmune syndrome characterized by T helper 1 (TH1) and
T helper 2 (TH2) CD4(+) T cell-dominated lesions. Here, we show that
pathogenic TH17 responses in mice are also restrained by Tregs. This
suppression was lost upon Treg-specific ablation of Stat3, a TF
critical for TH17 differentiation, and resulted in the development of
a fatal intestinal inflammation. These findings suggest that Tregs
adapt to their environment by engaging distinct effector response-
specific suppression modalities upon activation of STAT proteins that
direct the corresponding class of the immune response.
PMID: 19797626
Forget Unutmaz, Rudensky is rocking this sock puPPet.
I thought if i got littman and unutmaz on the same page it would be
COOL...
Let's bring some more of these science wiz kids to the forefront.
OK...
Looky we've got Runx... shades of Dr. Anne Bowcock time.
www.ncbi.nlm.nih.gov/pubmed/19767756
Runx-CBFbeta complexes control expression of the transcription factor
Foxp3 in regulatory T cells.
Rudra D, Egawa T, Chong MM, Treuting P, Littman DR, __Rudensky AY.___
Howard Hughes Medical Institute, University of Washington, Seattle,
Washington, USA.
The transcription factor Foxp3 has an indispensable role in
establishing stable transcriptional and functional programs of
regulatory T cells (T(reg) cells). Loss of Foxp3 expression in mature T
(reg) cells results in a failure of suppressor function, yet the
molecular mechanisms that ensure steady, heritable Foxp3 expression in
the T(reg) cell lineage remain unknown. Using T(reg) cell-specific
gene targeting, we found that complexes of the transcription factors
Runx and CBFbeta were required for maintenance of Foxp3 mRNA and
protein expression in T(reg) cells. Consequently, mice lacking
CBFbetab exclusively in the T(reg) cell lineage had a moderate
lymphoproliferative syndrome. Thus, Runx-CBFbeta complexes maintain
stable high expression of Foxp3 and serve as an essential determinant
of T(reg) cell lineage stability.
PMID: 19767756
This doesn't look like Bowcocks runx....
What is Runx/CBFbeta exactly?
Haven't a flying clue.
Do know:
http://en.wikipedia.org/wiki/RUNX1
[...]
Interactions
RUNX1 has been shown to interact with TLE1,[5] C-jun,[6][7] Calcitriol
receptor,[8] SUV39H1[9] and C-Fos.[6][7]
<sniP>
http://en.wikipedia.org/wiki/RUNX2
http://en.wikipedia.org/wiki/RUNX3
So CFB must BE
http://en.wikipedia.org/wiki/Core_binding_factor
Core binding factors (CBFs) comprise a group of heterodimeric
transcription factors.
They are composed of:
a non-DNA-binding CBFβ chain (CBFB)
a DNA-binding CBFα chain (RUNX1, RUNX2, RUNX3)
<sniP>
www.ncbi.nlm.nih.gov/pubmed/18681949
The evolutionary origin of the Runx/CBFbeta transcription factors--
studies of the most basal metazoans.
Sullivan JC, Sher D, Eisenstein M, Shigesada K, Reitzel AM, Marlow H,
Levanon D, Groner Y, Finnerty JR, Gat U.
Department of Biology, Boston University, 5 Cummington St, Boston, MA
02215, USA. jamescs...@gmail.com
BACKGROUND: Members of the Runx family of transcriptional regulators,
which bind DNA as heterodimers with CBFbeta, are known to play
critical roles in embryonic development in many triploblastic animals
such as mammals and insects. They are known to regulate basic
developmental processes such as cell fate determination and cellular
potency in multiple stem-cell types, including the sensory nerve cell
progenitors of ganglia in mammals. RESULTS: In this study, we detect
and characterize the hitherto unexplored Runx/CBFbeta genes of
cnidarians and sponges, two basal animal lineages that are well known
for their extensive regenerative capacity. Comparative structural
modeling indicates that the Runx-CBFbeta-DNA complex from most
cnidarians and sponges is highly similar to that found in humans, with
changes in the residues involved in Runx-CBFbeta dimerization in
either of the proteins mirrored by compensatory changes in the binding
partner. In situ hybridization studies reveal that Nematostella Runx
and CBFbeta are expressed predominantly in small isolated foci at the
base of the ectoderm of the tentacles in adult animals, possibly
representing neurons or their progenitors. CONCLUSION: These results
reveal that Runx and CBFbeta likely functioned together to regulate
transcription in the common ancestor of all metazoans, and the
structure of the Runx-CBFbeta-DNA complex has remained extremely
conserved since the human-sponge divergence. The expression data
suggest a hypothesis that these genes may have played a role in nerve
cell differentiation or maintenance in the common ancestor of
cnidarians and bilaterians.
PMID: 18681949 [PubMed - indexed for MEDLINE]
The whole study for the above abstract:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2527000/
www.ncbi.nlm.nih.gov/pubmed/19667061
Feedback control of regulatory T cell homeostasis by dendritic cells
in vivo.
Darrasse-Jèze G, Deroubaix S, Mouquet H, Victora GD, Eisenreich T, Yao
KH, Masilamani RF, Dustin ML, __Rudensky A,__ Liu K, Nussenzweig MC.
Laboratory of Molecular Immunology, The Rockefeller University, New
York, NY 10065, USA. gdar...@rockefeller.edu
CD4(+)CD25(+)Foxp3(+) natural regulatory T cells (T reg cells)
maintain self-tolerance and suppress autoimmune diseases such as type
1 diabetes and inflammatory bowel disease (IBD). In addition to their
effects on T cells, T reg cells are essential for maintaining normal
numbers of dendritic cells (DCs): when T reg cells are depleted, there
is a compensatory Flt3-dependent increase in DCs. However, little is
known about how T reg cell homeostasis is maintained in vivo. We
demonstrate the existence of a feedback regulatory loop between DCs
and T reg cells. We find that loss of DCs leads to a loss of T reg
cells, and that the remaining T reg cells exhibit decreased Foxp3
expression. The DC-dependent loss in T reg cells leads to an increase
in the number of T cells producing inflammatory cytokines, such as
interferon gamma and interleukin 17. Conversely, increasing the number
of DCs leads to increased T reg cell division and accumulation by a
mechanism that requires major histocompatibility complex II expression
on DCs. The increase in T reg cells induced by DC expansion is
sufficient to prevent type 1 autoimmune diabetes and IBD, which
suggests that interference with this feedback loop will create new
opportunities for immune-based therapies.
PMID: 19667061
www.ncbi.nlm.nih.gov/pubmed/19666573
Expression of GARP selectively identifies activated human FOXP3+
regulatory T cells.
Wang R, Kozhaya L, Mercer F, Khaitan A, Fujii H, __Unutmaz D.___
Department of Microbiology, NYU Cancer Institute and New York
University School of Medicine, New York, NY 10016, USA.
The molecules that define human regulatory T cells (Tregs)
phenotypically and functionally remain to be fully characterized. We
recently showed that activated human Tregs express mRNA for a
transmembrane protein called glycoprotein A repetitions predominant
(GARP, or LRRC32). Here, using a GARP-specific mAb, we demonstrate
that expression of GARP on activated Tregs correlates with their
suppressive capacity. However, GARP was not induced on T cells
activated in the presence of TGFbeta, which expressed high levels of
FOXP3 and lacked suppressive function. Ectopic expression of FOXP3 in
conventional T cells was also insufficient for induction of GARP
expression in most donors. Functionally, silencing GARP in Tregs only
moderately attenuated their suppressive activity. CD25+ T cells sorted
for high GARP expression displayed more potent suppressive activity
compared with CD25+GARP- cells. Remarkably, CD25+GARP- T cells
expanded in culture contained 3-5 fold higher IL-17-secreting cells
compared with either CD25+GARP+ or CD25-GARP- cells, suggesting that
high GARP expression can potentially discriminate Tregs from those
that have switched to Th17 lineage. We also determined whether GARP
expression correlates with FOXP3-expressing T cells in human
immunodeficiency virus (HIV) -infected subjects. A subset of HIV+
individuals with high percentages of FOXP3+ T cells did not show
proportionate increase in GARP+ T cells. This finding suggests that
higher FOXP3 levels observed in these HIV+ individuals is possibly due
to immune activation rather than to an increase in Tregs. Our findings
highlight the significance of GARP both in dissecting duality of Treg/
Th17 cell differentiation and as a marker to identify bona fide Tregs
during diseases with chronic immune activation.
PMID: 19666573
So we go back to Dec 2005 and psor runx with Dr. Bowcock:
www.ncbi.nlm.nih.gov/pubmed/16235096
Localization of PSORS1 to a haplotype block harboring HLA-C and
distinct from corneodesmosin and HCR.
Helms C, Saccone NL, Cao L, Daw JA, Cao K, Hsu TM, Taillon-Miller P,
Duan S, Gordon D, Pierce B, Ott J, Rice J, Fernandez-Vina MA, Kwok PY,
Menter A, Bowcock AM.
Department of Genetics, Washington University School of Medicine, Box
8232, 4566 Scott Avenue, St. Louis, Missouri, 63110, USA.
Psoriasis is a complex inflammatory disease of the skin affecting 1-2%
of the Caucasian population. Associations with alleles from the HLA
class I region (now known as PSORS1), particularly HLA-Cw*0602, were
described over 20 years ago. However, extensive linkage disequilibrium
(LD) within this region has made it difficult to identify the true
susceptibility allele from this region. A variety of genes and regions
from a 238-kb interval extending from HLA-B to corneodesmosin (CDSN)
have been proposed to harbor PSORS1. In order to identify the minimum
block of LD in the MHC class I region associated with psoriasis we
performed a comprehensive case/control and family-based association
study on 242 Northern European psoriasis families and two separate
European control populations. High resolution HLA typing of HLA-A, -B
and -C alleles was performed, in addition to the genotyping of 18
polymorphic microsatellites and 36 SNPs from a 772-kb segment of the
HLA class I region harboring the previously described interval. This
corresponded on average to one SNP every 7 kb in the candidate 238 kb
region. With all tests, the association was the strongest with single
markers and haplotypes from a block of LD harboring HLA-C and SNP n.9.
Logistic regression analyses indicated that association seen with
candidate genes from the interval such as CDSN and HCR was entirely
dependent on association with HLA-Cw*0602 and SNP n.9-G alleles. The
previously reported association with CDSN and HCR was observed to be
due to the existence of the associated alleles lying on the most
commonly over-transmitted haplotype. Rare over-transmitted haplotypes
also harbored HLA-Cw*12 alleles. HLA-Cw*12 family members are closely
related to HLA Cw*0602, sharing identical sequences in their alpha-2
domains, peptide-binding pockets A, D and E and all 3' introns. The
introduction of a potential binding site for the RUNX/AML family of
transcription factors in intron 7, is also specific to these HLA-C
alleles. These variants need to be investigated further for their role
as PSORS1.
PMID: 16235096
11 hits-- runx* + psoria* - pubmed:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=psoria*+AND+runx*&log$=activity
The most recent for psoria* + runx is march 6, 2006
www.ncbi.nlm.nih.gov/pubmed/16519819
Analysis of polymorphisms in 16 genes in type 1 diabetes that have
been associated with other immune-mediated diseases.
Smyth DJ, Howson JM, Payne F, Maier LM, Bailey R, Holland K, Lowe CE,
Cooper JD, Hulme JS, Vella A, Dahlman I, Lam AC, Nutland S, Walker NM,
Twells RC, Todd JA.
Juvenile Diabetes Research Foundation/Wellcome Trust Diabetes and
Inflammation Laboratory, Cambridge Institute for Medical Research,
Wellcome Trust/MRC Building, Addenbrooke's Hospital, Hills Rd,
Cambridge, CB2 2XY, UK. debbie...@cimr.cam.ac.uk
BACKGROUND: The identification of the HLA class II, insulin (INS),
CTLA-4 and PTPN22 genes as determinants of type 1 diabetes (T1D)
susceptibility indicates that fine tuning of the immune system is
centrally involved in disease development. Some genes have been shown
to affect several immune-mediated diseases. Therefore, we tested the
hypothesis that alleles of susceptibility genes previously associated
with other immune-mediated diseases might perturb immune homeostasis,
and hence also associate with predisposition to T1D. METHODS: We
resequenced and genotyped tag single nucleotide polymorphisms (SNPs)
from two genes, CRP and FCER1B, and genotyped 27 disease-associated
polymorphisms from thirteen gene regions, namely FCRL3, CFH, SLC9A3R1,
PADI4, RUNX1, SPINK5, IL1RN, IL1RA, CARD15, IBD5-locus (including
SLC22A4), LAG3, ADAM33 and NFKB1. These genes have been associated
previously with susceptibility to a range of immune-mediated diseases
including rheumatoid arthritis (RA), systemic lupus erythematosus
(SLE), Graves' disease (GD), psoriasis, psoriatic arthritis (PA),
atopy, asthma, Crohn disease and multiple sclerosis (MS). Our T1D
collections are divided into three sample subsets, consisting of set 1
families (up to 754 families), set 2 families (up to 743 families),
and a case-control collection (ranging from 1,500 to 4,400 cases and
1,500 to 4,600 controls). Each SNP was genotyped in one or more of
these subsets. Our study typically had approximately 80% statistical
power for a minor allele frequency (MAF) >5% and odds ratios (OR) of
1.5 with the type 1 error rate, alpha = 0.05. RESULTS: We found no
evidence of association with T1D at most of the loci studied 0.02 <P <
1.0. Only a SNP in ADAM33, rs2787094, was any evidence of association
obtained, P = 0.0004 in set 1 families (relative risk (RR) = 0.78),
but further support was not observed in the 4,326 cases and 4,610
controls, P = 0.57 (OR = 1.02). CONCLUSION: Polymorphisms in a variety
of genes previously associated with immune-mediated disease
susceptibility and/or having effects on gene function and the immune
system, are unlikely to be affecting T1D susceptibility in a major
way, even though some of the genes tested encode proteins of immune
pathways that are believed to be central to the development of T1D. We
cannot, however, rule out effect sizes smaller than OR 1.5.
PMID: 16519819 [PubMed - indexed for MEDLINE]
===================
OK, let's move in to the present day for runx...
Runx* aND lamina propria... it's a hot zone. LOL
40 hits for runx* + lamina propria
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=runx*+AND+lamina+propria&log$=activity
The first one should hopefully tell me something.
www.ncbi.nlm.nih.gov/pubmed/19665002
Helicobacter pylori causes runx3 gene methylation and its loss of
expression in gastric epithelial cells, which is mediated by nitric
oxide produced by macrophages.
Katayama Y, Takahashi M, Kuwayama H.
Department of Gastroenterology and Hepatology, Dokkyo Medical
University, Koshigaya Hospital, Saitama, Japan.
Previous reports have indicated that Helicobacter pylori (H. pylori)
causes epigenetic changes of certain genes such as cancer suppression
genes, which may be associated with carcinogenesis. However, the
mechanism by which it causes epigenetic changes in certain genes and
not in others is unclear. Presently, we focused on a cancer
suppression gene, runx3, and demonstrated the following: (1) H. pylori
induces nitric oxide (NO) production in macrophages. (2) NO causes
methylation of runx3 in epithelial cells. (3) H. pylori induces the
methylation of epithelial cells in the presence of macrophages, which
is reversed by an NO-specific inhibitor. These results indicate that
H. pylori-induced methylation is mediated by NO, and suggest that NO
may be a key to the mechanism of how H. pylori causes epigenetic
changes in certain genes. Additionally, we demonstrated that
lipopolysaccharide, as well as H. pylori, induces NO-mediated
methylation, indicating that other inflammation inducers beside H.
pylori might induce aberrant methylation of runx3.
PMID: 19665002
Runx3 GIT er DONE in the Gi tract?
www.ncbi.nlm.nih.gov/pubmed/19169278
Runx3 expression in gastrointestinal tract epithelium: resolving the
controversy.
Ito K, Inoue KI, Bae SC, Ito Y.
Institute of Molecular and Cell Biology, Proteos, Singapore.
We reported earlier that RUNX3 is expressed in human and mouse
gastrointestinal tract (GIT) epithelium and that it functions as a
tumor suppressor in gastric and colorectal tissues. However, there
have been conflicting reports describing the absence of Runx3 in GIT
epithelial cells. A part of the controversy may be derived from the
use of a specific antibody by other groups (referred to as G-poly).
Here, we show further evidence to support our earlier observations and
provide a possible explanation for this apparent controversy. We
generated multiple anti-RUNX3 monoclonal antibodies and found that
RUNX3 antibodies recognizing the RUNX3 N-terminal region (residues
1-234) react with RUNX3 in gastric epithelial cells, whereas those
recognizing the C-terminal region (beyond residue 234) did not. G-poly
primarily recognizes the region beyond 234 and hence, is unable to
detect Runx3 in this tissue.
PMID: 19169278
Ok, and now to crohn's for IL-17 machin- NOTIONs?
Ok,
www.ncbi.nlm.nih.gov/pubmed/18512248
IL-23/IL-17 immunity as a hallmark of Crohn's disease.
Hölttä V, Klemetti P, Sipponen T, Westerholm-Ormio M, Kociubinski G,
Salo H, Räsänen L, Kolho KL, Färkkilä M, Savilahti E, Vaarala O.
Laboratory for Immunobiology, Department of Viral Diseases and
Immunology, National Public Health Institute, Helsinki, Finland.
BACKGROUND: We studied the balance between ileal T-effector cells
versus T-regulatory cells in active and inactive Crohn's disease (CD).
METHODS: We compared effector and regulatory T-cell-related markers
such as interleukin (IL)-17, interferon (IFN)-gamma, IL-4, and Foxp3
transforming growth factor (TGF)-beta CTLA-4 and markers for innate
immune activation such as IL-6, IL-10, IL-18, IL-23, tumor necrosis
factor (TNF)-alpha, and IL-12p70, studied with immunohistochemistry
and RT-PCR in ileal biopsies from patients with active or inactive CD
and from control subjects. IL-17 in fecal samples was detected by
ELISA. The effect of IL-17 on IL-8 and TNF-alpha mRNA expression in
epithelial cell line Caco-2 was studied. RESULTS: The numbers of
IL-4-, IL-17-, and IL-23(p19)-positive cells in the lamina propria
were higher in patients with CD, both active and inactive, than in the
controls. mRNA expression of IL-17A, IL-6, and Foxp3 was increased in
the biopsies both from patients with active disease and those in
remission, whereas mRNA expression of IL-23 was increased only in
active disease. Fecal IL-17 concentration was increased in patients
with active disease. IL-17 enhanced the IL-8 and TNF-alpha response of
the epithelial cell line to lipopolysaccharide (LPS) in vitro.
CONCLUSIONS: Our findings suggest that activation of the IL-23/IL-17
axis is fundamentally connected to the etiology of CD and may
represent the basis for the relapsing nature of the disease by
increasing the sensitivity of epithelium to microbial LPS.
PMID: 18512248
All roads lead back to the sweet whey.. and more lacti loving bugs to
re-regulate
all Gi tract flora.
So how do we get the GIT bugs back in?
Like L. plantarum?
Yes...
http://en.wikipedia.org/wiki/Lactobacillus_plantarum
How much LAB do we eat?
Or is eating gonna work?
http://en.wikipedia.org/wiki/Lactic_acid_bacteria
http://www.examiner.co.uk/news/local-west-yorkshire-news/2009/11/07/do-probiotic-yoghurt-drinks-make-you-healthier-scientists-from-the-university-of-huddersfield-have-their-say-86081-25110741/
Do probiotic yoghurt drinks make you healthier? Scientists from the
University of Huddersfield have their say
Nov 7 2009 by John Avison, Huddersfield Daily Examiner
TV, radio and newspapers are awash with adverts for ‘probiotic’
yoghurt products.
It’s been assumed that anything that boosts ‘good’ bacteria in the
stomach and gut is beneficial.
But now scientists at the European Food Safety Agency (EFSA) have
announced that there is little evidence to support the health benefits
of probiotic products.
[randall note: Duh... you have to do the wit kit and a rectal implant
and diet.... duh]
And only a couple of weeks ago, the Advertising Standards Authority
refused to allow a new advert suggesting that children who consume
probiotic yoghurts will boost their natural defence mechanisms.
The claim that probiotics are giving health benefits are being
challenged and Huddersfield University scientists are leading the
charge.
For two decades, the university has been at the forefront of research
into the human body’s complex relationship with its bacteria.
This research got a huge boost a decade ago with a £1m EU grant and
university scientists comprise one of the few UK teams to study the
molecular structure of the bacteria in the stomach and gut.
“We are building a picture of the bacteria that communicate with the
immune system and the chemical messengers they use,” said Dr Andy
Laws, a reader in chemistry at the university’s department of
chemistry and biology.
“Research is now putting more emphasis on ‘prebiotics’, (non-
digestible food fibres and complex sugars) on which bacteria feed.”
There are between 4,000 and 500 different kinds of bacteria in the
gut, some good and some bad.
You can distinguish and to an extent ‘sculpt’ the prebiotics to help
the good bacteria thrive and deprive the bad bacteria of nourishment.
This, rather than the indiscriminate bombardment of the gut with
probiotics, might be the way forward, says Dr Laws.
“The manufacturers of probiotics have met problems in which their
products have had an adverse effect on the stomach, creating excess
wind,” he said.
“So should we rush to consume probiotic yoghurts? The answer is not
clear.
“If you have a good diet then your gut bacteria should be strong
enough to supply the immune response needed to keep you healthy.
“There is evidence in the scientific literature to suggest that the
consumption of probiotic drinks can be advantageous when the normal
gut flora has been damaged, such as after antibiotic treatment.”
“At the same time, there are a limited number of reports that the
consumption of too many probiotic strains – particularly by people who
have serious medical conditions such as pancreatitis – can have
negative effects.
“This is an area of research which we urgently need to develop. We
need to know how the communication between the normal gut flora and
the immune system works.”
One of the most common causes of a breakdown in this communication is
after treatment with antibiotics.
Often elderly patients who have bacterial infections are given broad
spectrum antibiotics that help them tackle infections.
However, these antibiotics also kill a significant proportion of the
normal healthy gut flora.
This gives resistant strains of bad bacteria, notably C. difficile,
the opportunity to colonise the gut with the consequence that patients
experience so called ‘antibiotic’ induced diarrhoea.
There are also a number of severe diseases where there is believed to
be the result of poor communication between the bacteria and the
immune system.
Crohn’s disease and inflammatory bowel disease are the most notable
here.
We often think of bacteria as harmful organisms, but while many do
cause disease, some are beneficial to the body.
Since the majority of these bacteria are in the gut, the gut can be
viewed as the body’s largest immune organ with the biggest
responsibility for fending off harmful organisms known as pathogens.
Good bacteria also plays another important role, breaking down food we
eat to provide a source of energy essential for the cells that line
the intestines.
Yet another benefit is that good bacteria helps to make vitamins
needed by the body and keep the digestive system working as it should.
Probiotics like lactobacilli plantarum and bifidobacteria, which are
favoured by the therapeutic yoghurt makers, are present naturally in
fruit and vegetables, but you have to eat massive amounts each day for
the bacteria to have an effect.
And, indeed, if you choose to take Actimel, Muller or other products,
the benefits will only be felt if you take them regularly.
One live yoghurt just isn’t enough to repopulate your intestines with
healthy bacteria.
Dr Trisha Mcnair, the BBC’s health adviser, said: “It may be more
effective to take prebiotics that boost growth of the good bacteria
you already have in your gut, rather than take supplements of live
bacteria that may be destroyed by the acidity of the stomach as soon
as you swallow them.”
===========================
How do we get all of these scientists to come together and say i'm
right. LOL
The wit kit is the best way to promote lactic acid bacteria (LAB) in
the colon and
that will re-regulate the colon to become slightly acidic and that
will clean up
the stuff just north of colon in the ileum to downregulate the SFB's.
Segmented Filamentous bacterium trials are starting SOON..
And i'm the only one doing that ....
randall.... kicks it... LOL
scientist123foxp3
hilarious.