Curcumin -- SFB - ILEUM -- Considerations
randall
Let's say that curcumin does ALL the good things we read about.
How many hit's in OUR group for instance?
1,010 hits for keyword: curcumin [in the psoriasis newsgroup]
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&group=alt.support.skin-diseases.psoriasis&q=curcumin
So why doesn't it CLEAR JRSTERN?
He admits that IT helps but NOT enough to make a REAL difference
beyond
KNOWing that something is helping.
So?
www.ncbi.nlm.nih.gov/pubmed/19839007
Curcumin induces the tolerogenic dendritic cell that promotes
differentiation of intestine-protective regulatory T cells.
Cong Y, Wang L, Konrad A, Schoeb T, Elson CO.
Division of Gastroenterology and Hepatology, Department of Medicine,
Birmingham, AL, USA.
The gut is home to a large number of Treg, with both CD4(+) CD25(+)
Treg and bacterial antigen-specific Tr1 cells present in normal mouse
intestinal lamina propria. It has been shown recently that intestinal
mucosal DC are able to induce Foxp3(+) Treg through production of TGF-
beta plus retinoic acid (RA). However, the factors instructing DC
toward this mucosal phenotype are currently unknown. Curcumin has been
shown to possess a number of biologic activities including the
inhibition of NF-kappaB signaling. We asked whether curcumin could
modulate DC to be tolerogenic whose function could mimic mucosal DC.
We report here that curcumin modulated BM-derived DC to express ALDH1a
and IL-10. These curcumin-treated DC induced differentiation of naïve
CD4(+) T cells into Treg resembling Treg in the intestine, including
both CD4(+)CD25(+) Foxp3(+) Treg and IL-10-producing Tr1 cells. Such
Treg induction required IL-10, TGF-beta and retinoic acid produced by
curcumin-modulated DC. Cell contact as well as IL-10 and TGF-beta
production were involved in the function of such induced Treg. More
importantly, these Treg inhibited antigen-specific T-cell activation
in vitro and inhibited colitis due to antigen-specific pathogenic T
cells in vivo.
PMID: 19839007
Curcumin promotes IL-10 and TREG's. Both help to slow psoriasis.
So why doesn't it do more? For you, i and JRSTERN?
Maybe because we keep feeding SFB (segmented filamentous bacteria) and
it pumps out Th17 (Th-17) faster then IL-10 and TREG's can do their
JOB?
Makes sense to me.
Time will tell..
IN this next abstract Treg's increased with levels of inflammation...
----
Foxp3-expressing T regulatory cells and mast cells in acute graft-
versus-host disease of the skin.
Wu KN, Emmons RV, Lisanti MP, Farber JL, Witkiewicz AK.
Department of Pathology, Thomas Jefferson University, Philadelphia,
PA, USA.
Acute graft-versus-host disease (aGVHD) limits the effectiveness of
allogeneic hematopoietic stem cell transplantation. Foxp3 is required
for the development and function of CD4(+)/CD25(+) regulatory T cells
(T-regs). Foxp3-expressing T-regs are thought to protect against GVHD.
Mast cells are thought to be essential in CD4(+)/CD25(+) regulatory T
cell-dependent peripheral tolerance. Twenty biopsies of skin with
grades I-III aGVHD were stained for Foxp3 and CD117. Inflammation was
quantified by a 4 point scale, 0 = no inflammation, 1 = <25% of 20x
field, 2 = 25-50%, and 3 = >50%. T-regs and mast cells were quantified
by a 4 point scale, 0 = no cells per 20x field, 1 = <5 cells per 20x
field, 2 = 5-10 cells, and 3 = >10 cells. T-regs were positively
correlated with both inflammation and aGVHD grade. Twelve cases with
low T-regs had mild inflammation and lower grades of aGVHD and 6 cases
with high T-regs had dense inflammatory infiltrate and higher grades
of aGVHD. The number of T-regs, mast cells and density of the
inflammatory infiltrate were positively correlated only in cases with
mild inflammation. In aGVHD of the skin, T-regs increased with the
degree of inflammation and GVHD grade. Mast cells were present at the
same density whether aGVHD was of lower or higher grade.
PMID: 19838066
So why doesn't TREG's increase with severe inflammation of psoriasis?
Maybe becasue NO ONE has correlated it with amounts of SFB in the
ileum?
WE DO have 10 hits for keywords::: ileum + SFB [on pubmed]
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=ileum+SFB&log$=activity
The first two have been posted at least a few times in the last week.
SEE:
Induction of Intestinal Th17 Cells by Segmented Filamentous Bacteria.
www.ncbi.nlm.nih.gov/pubmed/19836068
&
A strain of Lactobacillus plantarum affects segmented filamentous
bacteria in the intestine of immunosuppressed mice.
www.ncbi.nlm.nih.gov/pubmed/18081591
THEN:
www.ncbi.nlm.nih.gov/pubmed/17995961
Differential effects of two probiotic strains with different
bacteriological properties on intestinal gene expression, with special
reference to indigenous bacteria.
Shima T, Fukushima K, Setoyama H, Imaoka A, Matsumoto S, Hara T, Suda
K, Umesaki Y.
Yakult Central Institute for Microbiological Research, Kunitachi-shi,
Tokyo, Japan.
Probiotics are used for the improvement of gut disorders. To explore
the potential of probiotics, a gnotobiotic study using BALB/c mice to
analyze epithelial gene expression was performed. Microarray analysis
of probiotic strain-monoassociated mice showed that Lactobacillus
casei Shirota and Bifidobacterium breve Yakult noticeably affected
gene expression in the ileal and colonic epithelial cells,
respectively, although to a smaller extent than segmented filamentous
bacteria (SFB). Lactobacillus casei Shirota enhanced the gene
expression involving defense/immune functions and lipid metabolism
more strongly than B. breve Yakult. In the colon, expression of a
chloride transporter was slightly enhanced, although downregulation of
many genes, such as guanine nucleotide-binding protein, was evident in
mice with B. breve Yakult compared with the ones with L. casei
Shirota. SFB affected gene expression more strongly than the probiotic
strains. In particular, alpha(1-2) fucosyltransferase and pancreatitis-
associated protein were significantly enhanced only in SFB-
monoassociated mice but not probiotic strain-monoassociated mice. Gene
expression of SFB-monoassociated mice was either stimulated or
repressed in a manner similar to or opposite that of conventional
colonized mice. Taken together, probiotic strains of L. casei Shirota
and B. breve Yakult differentially affect epithelial gene expression
in the small intestine and colon, respectively.
PMID: 17995961
Segmented filamentous bacteria in a defined bacterial cocktail induce
intestinal inflammation in SCID mice reconstituted with CD45RBhigh
CD4+ T cells.
Stepankova R, Powrie F, Kofronova O, Kozakova H, Hudcovic T, Hrncir T,
Uhlig H, Read S, Rehakova Z, Benada O, Heczko P, Strus M, Bland P,
Tlaskalova-Hogenova H.
Laboratory of Gnotobiology, Department of Immunology, Institute of
Microbiology, Czech Academy of Sciences, Novy Hradek, Czech Republic.
stepanko...@seznam.cz
BACKGROUND: The aim was to analyze the influence of intestinal
microbiota on the development of intestinal inflammation. We used the
model of chronic inflammation that develops spontaneously in the colon
of conventional severe combined immunodeficiency (SCID) mice restored
with the CD45 RB(high) subset of CD4+T cells isolated from the spleen
of normal BALB/c mice. METHODS: A CD4+CD45RB(high) subpopulation of T
cells was purified from the spleen of conventional BALB/c mice by
magnetic separation (MACS) and transferred into immunodeficient SCID
mice. Germ-free (GF) SCID mice or SCID mice monoassociated with
Enterococcus faecalis, SFB (segmented filamentous bacteria),
Fusobacterium mortiferum, Bacteroides distasonis, and in combination
Fusobacterium mortiferum + SFB or Bacteroides distasonis + SFB were
used as recipients. SCID mice were colonized by a defined cocktail of
specific pathogen-free (SPF) bacteria. Mice were evaluated 8-12 weeks
after the cell transfer for clinical and morphological signs of
inflammatory bowel disease (IBD). RESULTS: After the transfer of the
CD4+CD45RB(high) T-cell subpopulation to SCID mice severe colitis was
present in conventional animals and in mice colonized with a cocktail
of SPF microflora plus SFB. Altered intestinal barrier in the terminal
ileum of mice with severe colitis was documented by immunohistology
using antibodies to ZO-1 (zona occludens). CONCLUSIONS: Only SFB
bacteria together with a defined SPF mixture were effective in
triggering intestinal inflammation in the model of IBD in
reconstituted SCID mice, while no colitis was detected in GF mice or
in mice colonized either with SPF microflora or monoassociated only
with SFB or colonized by Bacteroides distasonis + SFB or Fusobacterium
mortiferum + SFB.
PMID: 17607724
Segmented filamentous bacteria interact with intraepithelial
mononuclear cells.
Meyerholz DK, Stabel TJ, Cheville NF.
Department of Veterinary Microbiology and Preventive Medicine, Iowa
State University, Ames, Iowa 50010, USA.
Segmented filamentous bacteria (SFB) are found in multiple species and
play an important role in the development of mucosal immunity. The
mechanism by which the bacteria interact with the immune system has
not been well defined. We provide morphologic evidence of direct
interaction between SFB and intraepithelial mononuclear cells.
PMID: 12011024
CRAP... wish I saw this seven years ago. LOL
BACK to 1992:
Intestinal, segmented, filamentous bacteria.
Klaasen HL, Koopman JP, Poelma FG, Beynen AC.
Central Animal Laboratory, Catholic University of Nijmegen,
Netherlands.
Segmented, filamentous bacteria (SFBs) are autochthonous, apathogenic
bacteria, occurring in the ileum of mice and rats. Although the
application of formal taxonomic criteria is impossible due to the lack
of an in vitro technique to culture SFBs, microbes with a similar
morphology, found in the intestine of a wide range of vertebrate and
invertebrate host species, are considered to be related. SFBs are
firmly attached to the epithelial cells of the distal ileal mucosa,
their preferential ecological niche being the epithelium covering the
Peyer's patches. Electron microscopic studies have demonstrated a
considerable morphological diversity of SFBs, which may relate to
different stages of a life cycle. Determinants of SFB colonization in
vivo are host species, genotypical and phenotypical characteristics of
the host, diet composition, environmental stress and antimicrobial
drugs. SFBs can survive in vitro incubation, but do not multiply. On
the basis of their apathogenic character and intimate relationship
with the host, it is suggested that SFBs contribute to development and/
or maintenance of host resistance to enteropathogens.
PMID: 1515159
Koopman seems to be in several of these:
Mono-association of mice with non-cultivable, intestinal, segmented,
filamentous bacteria.
Klaasen HL, Koopman JP, Van den Brink ME, Van Wezel HP, Beynen AC.
Arch Microbiol. 1991;156(2):148-51.
PMID: 1838241
======================
59 hits for keywords:: ileum + Th1
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=ileum+Th1&log$=activity
That says enough for me.
I'll read a few of these within the next 24 hours.
I hope that JrSTERN looks long and hard at these.
Because it explains more then a few things to me.
And while certainly psor genetics are important, the SFB explains
onset and
quite a bit more, i'd bet.
And it is simple and elegant.
And we have 71 hits for keyword: ILUM [in our psor group]
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&group=alt.support.skin-diseases.psoriasis&q=ileum&qt_g=Search+this+group
If I'm wrong my next trial will certainly let me know as i plan to eat
the cure.
Or imPlant it. LOL
randall
JRStern
wrote:
>So why doesn't it do more? For you, i and JRSTERN?
Could be simple dosage in my case, I'm still using turmeric and
inching up the dosage. Adding n-3 and C seems to have helped. I'm
doing better than I have for some years, but there's not enough of mes
to try all the combinations.
Nobody says that TNF or Th-17 is the root cause, what *causes* them to
be in excess? Something upstream triggers the immune system to
overproduce them.
The wrong bacteria in your gut? Well, I suppose it's *possible*, but
seems unlikely, that the effects then show up pretty much only in your
skin, in symmetric patches, etc. If you just filled a person or a
mouse or whatever with a bunch of TNF in the gut, would that cause
them to have psoriasis?
Bacteria to gut permeability to something bad circulating and landing
in the skin and triggering a reaction, seems mildly more likely to me,
but we still have to account for hereditability. Well, I suppose one
can inherit bad skin and/or bad gut, and then have this complex
process light them up.
J.
randall
> On Wed, 21 Oct 2009 00:25:50 -0700 (PDT), randall <ranhu...@aol.com>
> wrote:
>
> >So why doesn't it do more? For you, i and JRSTERN?
>
> Could be simple dosage in my case, I'm still using turmeric and
> inching up the dosage.
But i did DO four to eight grams a day and more without enough
help to keep my attention.
Same thing with D3.
653 hits for keywords: randall + D3 [in our group alone]
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&group=alt.support.skin-diseases.psoriasis&q=randall+d3
> Adding n-3 and C seems to have helped. I'm
> doing better than I have for some years, but there's not enough of mes
> to try all the combinations.
So do what i do.
If sweet whey keeps the good flora high enough to lay a biofilm over
the crappy Gut flora it slows Th17 formation, perhaPs?
If it doesn't do that then simply having an slightly acidic gut must
ALLOW the good bacteria to hide (be a biofilm) in the appendix.
You KNOW next to the cecum. LOL
>
> Nobody says that TNF or Th-17 is the root cause, what *causes* them to
> be in excess? Something upstream triggers the immune system to
> overproduce them.
RIGHT i'm betting that SFB just like h. pylori is that causal factor.
How can you NOT get THAT?
I'm saying that bio ILL logicals are NOT LOGICAL because they don't
treat a CAUSE.
It's like putting out a fire while adding fuel to it.
Or driving a car with one foot pushing the brake and the other giving
it the GAS.
Why not use sweet WHEY to biofilm over the fire of putrefactive
bacteria?
It's like smothering a FIRE with retardant.
If SFB are the embers of our discontent and fits our PSOR genetics
then so much the BETTER.
AT least will NOT be Bitter. LOL
>
> The wrong bacteria in your gut? Well, I suppose it's *possible*, but
> seems unlikely, that the effects then show up pretty much only in your
> skin, in symmetric patches, etc.
I KNOW.... that must be the nature of CRAP or clusters of
differentiation?
http://en.wikipedia.org/wiki/Cluster_of_differentiation
Due to GENETICS of psors1 (MHC)
443 hits keywords: randall + mhc
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&group=alt.support.skin-diseases.psoriasis&q=randall+mhc
> If you just filled a person or a
> mouse or whatever with a bunch of TNF in the gut, would that cause
> them to have psoriasis?
Sure helps if you first only choose the psoriaform mice. LOL
Don't they have to be front loaded?
But if you front load them with good flora would the TNF
make the same impact?
http://www.pressandjournal.co.uk/Article.aspx/1431709?UserKey=
[...]
They also found that a protein in bacteroides thetaiotaomicron – a
friendly gut bacteria – triggers an anti-inflammatory response.
<sniP>
Denise Kelly looks like a major FOX.
She can plug my leaky gut any day of the week. LOL
>
> Bacteria to gut permeability to something bad circulating and landing
> in the skin and triggering a reaction, seems mildly more likely to me,
> but we still have to account for hereditability. Well, I suppose one
> can inherit bad skin and/or bad gut, and then have this complex
> process light them up.
>
> J.
Alright. I won you over. LOL :)
Now that your mind is prime it's TIME to obey the gosPel of galactose.
SWEET..
randall....what a whey to GO....
zzznot
news:1f84d9e3-6c70-4ae2...@j9g2000vbp.googlegroups.com...
> > Could be simple dosage in my case, I'm still using turmeric and
> > inching up the dosage.
>
> But i did DO four to eight grams a day and more without enough
> help to keep my attention.
Do you think then, maybe, we don't react the same to stuff?
Actually, talking turmeric, I saw definite small improvements
down around two to four grams, much better around eight, and I'm
sliding up to a (by-gosh measured) ten to fifteen these days.
I only recently became clear that the eight grams a day I've seen
in the literature, is eight grams of curcumin, which is more like
twenty-four of turmeric.
I suppose I should switch to the standardized curcumin, since
the combination of by-gosh measurement and probable variation in
turmeric/curcumin concentrations, is hard (eg impossible) to track.
J.
randall
> "randall" <ranhu...@aol.com> wrote in message
>
> news:1f84d9e3-6c70-4ae2...@j9g2000vbp.googlegroups.com...
>
> > > Could be simple dosage in my case, I'm still using turmeric and
> > > inching up the dosage.
>
> > But i did DO four to eight grams a day and more without enough
> > help to keep my attention.
>
> Do you think then, maybe, we don't react the same to stuff?
NO.... i thought and do now that i'm the perfect early onset
specimin for psoriatic tests.
Why should I let that be put to waste in double blind trials?
And if you used my wit kit and was clear right now, then you'd
understand exactly where i'm coming from.
Duh...
>
> Actually, talking turmeric, I saw definite small improvements
> down around two to four grams, much better around eight, and I'm
> sliding up to a (by-gosh measured) ten to fifteen these days.
> I only recently became clear that the eight grams a day I've seen
> in the literature, is eight grams of curcumin, which is more like
> twenty-four of turmeric.
OK, so why didn't you post this sooner?
Worried we all get really CLEAR?
I've never held back from day one.
I don't give a rats behind what the reality has
behind it.
I'm in to telling the truth and being FREE of psor plaques.
And if enough of you guys and gals join me then we'll all BE FREE.
And if susan doesn;t like it because it's not exactly a hpa-axis
control
over psoriasis then so what?
I still respect her and always will....
>
> I suppose I should switch to the standardized curcumin, since
> the combination of by-gosh measurement and probable variation in
> turmeric/curcumin concentrations, is hard (eg impossible) to track.
Why bother?
Why don't you follow me?
I gave it up and moved on.
And i'm nearly CLEAR,
Without it.
Why is that?
Because it's BS.
The same as that barney jerk wad.
I almost fell for his peppermint till til
susan put me STRAIGHT. LOL
So, get over it
And move to the light little one. :)
Randall... the light master... <G>
>
> J.
randall
> x-no-archive: yes
>
> randall wrote:
> > And if susan doesn;t like it because it's not exactly a hpa-axis
> > control
> > over psoriasis then so what?
>
> > I still respect her and always will....
>
>
> Susan
Dear Susan,
Thank-you for your faith in a CURE someday.
It could happen anytime. I'm SUrE.
Or Fur Sure... LOL
Crikey. The GAME is over it looks like.
Oh no. Rivera got a double in the top of the 8th.
I just need to wait for this Cialis ad to finish so i can
see what happened exactly...
I hate that, when the moment is right and their, if your
erection last longer then 244 hours see a doctor. LOL
What teenager ever said to his doctor i've got a
48 hour hard ON that just won't go away. LOL
They usually take matter's in to their own hands. LOL
randall... like me with my psor spots...