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From: Kofi on 14 May 2007 21:39
In the last year, allergic rhinitis has been linked to abnormal immune
reactions to the chitin produced by fungi and mites in sinus passages.
While looking through the butyrate literature, I came across an old
reference to the ability of butyrate to reduce chitin production in
yeast cells (Candida albicans).

Butyrate is produced by some bacteria when they digest dietary fiber.
Yeast and bacteria live side by side on surfaces of the human body like
the lining of the intestines where they compete for nutrients and help
the body digest food and manufacture vitamins. Normally these organisms
stay in balance due to this competition but heavy antibiotic exposure
can throw that balance out of whack and lead to fungal infections and
allergies. Butyrate provides a common, underlying link connecting
rhinitis, allergies and mold sensitivity.

Butyrate stimulates regulatory T-cells. A drop in Tregs can cause
autoimmunity whereas boosting their numbers and function alleviates
autoimmune symptoms - like, theoretically, a mold allergy. Butyrate
also reduces chitin production. Killing the bacteria which produce
butyrate would then encourage autoimmunity/allergy and prompt more
chitin production by surviving yeast, thus affecting individuals
predisposed to be sensitive to the higher levels of chitin. (By the
way, many of these bacteria themselves have anti-inflammatory, calming
influences on the immune system. The body recognizes fragments of their
genetic code or cell surface chemicals and turns off its inflammatory
reactions.)

It's just a theory I've cobbled together but it fits the facts fairly
well. I've certainly noticed a drop in my allergies and runny nose
while taking butyrate and carnitine. This may explain part of it.
Correlation doesn't establish causation but these coincidences point to
an hypothesis worthy of wider testing.


Am J Rhinol. 2006 May-Jun;20(3):330-5.
�
Increased expression of acidic mammalian chitinase in chronic
rhinosinusitis with nasal polyps.

Ramanathan M Jr, Lee WK, Lane AP.

Department of Otolaryngology-Head and Neck Surgery, The Johns Hopkins
University School of Medicine, Baltimore, Maryland 21287-0910, USA.

BACKGROUND: Chitin is an abundant polysaccharide found in fungi,
insects, and parasitic nematodes. Innate immune host defense against
chitin-containing pathogens include production of chitinases. In human
lower airways, acidic mammalian chitinase (AMCase) is produced in
epithelial cells via a Th2-specific, IL-13-dependent pathway, and may
act as an inflammatory mediator in asthma. The role of AMCase in chronic
rhinosinusitis (CRS) has not been studied previously. METHODS: Eleven
controls and 22 subjects with medically recalcitrant CRS were
prospectively enrolled before undergoing endoscopic sinus surgery. RNA
was extracted from surgically obtained ethmoid mucosa, and real-time PCR
was used to determine expression of AMCase, eotaxin, and IL-13. Subjects
were followed for at least 6 months postoperatively to assess for polyp
recurrence. Based on the presence or absence of polyps, the subjects
were classified as either recalcitrant or responsive to therapy.
RESULTS: AMCase mRNA was detected in the sinus mucosa of 72% of control
subjects and in 72% of patients with eosinophilic CRS with nasal polyps
(CRSwNP). The expression of AMCase was significantly greater in
recalcitrant CRSwNP than it was in treatment-responsive CRSwNP. There
was no significant difference in IL-13 expression between these two
groups. CONCLUSION: AMCase may be an important mediator in the
pathogenesis of Th2 inflammatory diseases of the respiratory tract.
Failure of medical and surgical therapy in CRSwNP is associated with
significantly increased expression of AMCase, but not the Th2 cytokines
IL-13 and eotaxin. Additional studies are needed to determine the
potential of AMCase as a therapeutic target in CRSwNP.

Publication Types:
* Research Support, Non-U.S. Gov't

PMID: 16871939


Can J Microbiol. 1987 Jun;33(6):546-50.

Effect of cerulenin and sodium butyrate on chitin synthesis in Candida
albicans.

Braun PC, Hector RF, Kamark ME, Hart JT, Cihlar RL.

Experiments were conducted to gain insight concerning the mechanism(s)
whereby cerulenin and sodium butyrate affect chitin synthesis in Candida
albicans. In vitro studies with isolated membrane-bound chitin synthase
from C. albicans, strain 4918, showed that neither agent affected the
level of either unactivated or trypsin-activated enzyme activity.
Subsequent studies utilizing protoplasts revealed that early in the cell
wall regeneration process, cells treated with cerulenin or butyrate
synthesized chitin at a rate equal to untreated controls, as measured by
the incorporation of [3H]-N-acetylglucosamine (GlcNAc) into acid-alkali
insoluble material. However, after 40 min of incubation, the
incorporation of [3H]GlcNAc into chitin is reduced in cells treated with
either agent. On the other hand, samples taken during the same time
intervals and analyzed by flow cytometry suggested that the amount of
chitin synthesis in treated and untreated cells was identical. A marked
decrease in fluorescence was observed in similar experiments using
polyoxin D, a direct inhibitor of chitin synthase activity. Experiments
that measured uptake of [3H]GlcNAc into both whole cells and protoplasts
demonstrated that cerulenin and butyrate had no effect on the transport
of the chitin precursor.

Publication Types:
* Research Support, Non-U.S. Gov't
* Research Support, U.S. Gov't, P.H.S.

PMID: 2957042 [PubMed - indexed for MEDLINE]


Antimicrob Agents Chemother. 1983 Sep;24(3):401-8.
��
Inhibitory effect of cerulenin and sodium butyrate on germination of
Candida albicans.

Hoberg KA, Cihlar RL, Calderone RA.

Candida albicans germination in liquid medium was inhibition by the
antilipogenic agent cerulenin and the fatty acid sodium butyrate.
Although these inhibitors prevented germ tube emergence at
concentrations of 1 microgram/ml and 20 mM, respectively, neither
significantly affected cell viability as judged by trypan blue staining
or the rate of protein biosynthesis throughout the time course of the
experiments. Cerulenin treatment resulted in inhibition of lipid
biosynthesis, but lipid biosynthetic capabilities remained unaltered in
sodium butyrate-supplemented cultures. Because each inhibitor blocks
germination by different mechanisms, their utility in distinguishing
events directly correlated to germination was examined. In this context,
chitin synthase activity was inhibited by both compounds, confirming the
importance of chitin biosynthesis in C. albicans germination.

Publication Types:
* Research Support, Non-U.S. Gov't
* Research Support, U.S. Gov't, P.H.S.

PMID: 6357077
From: Pouta on 14 May 2007 23:52
> I've certainly noticed a drop in my allergies
> and runny nose while taking butyrate and
> carnitine.

I take it your G.I. tract is tolerating this combo
well...? are you taking these with food, or on
an empty stomach ? (I ask this because I've
read that free-form amino acids are best
absorbed if taken before meals)






From: truehawk on 15 May 2007 01:27
>'It's just a theory I've cobbled together but it fits the facts fairly
>well. I've certainly noticed a drop in my allergies and runny nose
>while taking butyrate and carnitine. This may explain part of it.
>Correlation doesn't establish causation but these coincidences point to
>an hypothesis worthy of wider testing. '

Sounds promising.

But what were they thinking writing this:

>RESULTS: AMCase mRNA was detected in the sinus mucosa of 72% of control
>subjects and in 72% of patients with eosinophilic CRS with nasal polyps
>(CRSwNP).

They SERIOUSLY need a proofreader at Hopkins.
72% of controls have AMCase mRNA.
and 72% of patients with eosinophilic CRS with nasal polyps (CRSwNP)
have it.
Looks like there is NO difference in AMCase mRNA expression between
the two groups.
Is this a typo or is there no difference between the AMCase mRNA
status of healthy and sick people?
>From this abstract one can't really tell.

Cause the next thing they say is

>The expression of AMCase was significantly greater in
>recalcitrant CRSwNP than it was in treatment-responsive CRSwNP.

Okay, but where are the %s for the respective groups?
because the two %s they gave don't show any difference at all.

I am not saying that there is not a valid result here somewhere, but
what was it?

From: Kofi on 15 May 2007 23:30
In article <1179201178.506408.178140(a)n59g2000hsh.googlegroups.com>,
Pouta <aquarius_122(a)hotmail.com> wrote:

> > I've certainly noticed a drop in my allergies
> > and runny nose while taking butyrate and
> > carnitine.
>
> I take it your G.I. tract is tolerating this combo
> well...? are you taking these with food, or on
> an empty stomach ? (I ask this because I've
> read that free-form amino acids are best
> absorbed if taken before meals)

I'm taking the combination with food. I also take some carnitine HCl
and other amino acids on an empty stomach. It's very helpful.
From: Kofi on 15 May 2007 23:37
They noted AMCase mRNA was present in both groups in the first
comparison (namely, 72% of each group were positive for it), but they
didn't state how much that mRNA was being expressed until they compared
groups postsurgery, where they linked severity of the condition to the
amount of AMCase mRNA.

What's even more confusing is that strands of mRNA don't determine
absolutely how much of a protein is getting made. One cell with less
mRNA for a certain protein can actually make more of that protein than
other cells with more mRNA if other aspects of protein synthesis are
kicked into high gear.
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