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Butyrate from gut bacteria inhibits chitin production in yeast; link to rhinitis

by Kofi <kofi@[EMAIL PROTECTED] > May 15, 2007 at 01:39 AM

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 *****s 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 im****tant 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 Sup****t, 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 incor****ation of [3H]-N-acetylglucosamine (GlcNAc) into acid-alkali 
insoluble material. However, after 40 min of incubation, the 
incor****ation 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 trans****t 
of the chitin precursor.

Publication Types: 
*  Research Sup****t, Non-U.S. Gov't 
*  Research Sup****t, 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 distingui****ng 
events directly correlated to germination was examined. In this context, 
chitin synthase activity was inhibited by both compounds, confirming the 
im****tance of chitin biosynthesis in C. albicans germination.

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

PMID: 6357077
 




 5 Posts in Topic:
Butyrate from gut bacteria inhibits chitin production in yeast;
Kofi <kofi@[EMAIL PROT  2007-05-15 01:39:12 
Re: Butyrate from gut bacteria inhibits chitin production in yea
Pouta <aquarius_122@[E  2007-05-14 20:52:58 
Re: Butyrate from gut bacteria inhibits chitin production in yea
Kofi <kofi@[EMAIL PROT  2007-05-16 03:30:35 
Re: Butyrate from gut bacteria inhibits chitin production in yea
truehawk <truehawk@[EM  2007-05-14 22:27:18 
Re: Butyrate from gut bacteria inhibits chitin production in yea
Kofi <kofi@[EMAIL PROT  2007-05-16 03:37:01 

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