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Celiac disease, IBS, Crohn's disease, hypochlorhydria (low stomach acid),
as well as antibiotic use, can all disturb the mix of gut microflora.  This
can be a significant factor in the development of food allergies.  A new
study lends further support to the importance of maintaining a healthy mix
of gut flora to ward-off food allergies.

Toll-like receptors (TLR), located on the surface dendritic cells,
epithelial cells and other immune system cells, sense structural components
found only on the surface of bacteria and other pathogens.  They are
important as to how the immune system responds to microflora inhabiting the
gut.  There are at least 10 types of Toll-like receptors in humans
(recently an 11th was identified) which identify specific kinds of
bacterial components.  The following study now has found an association
between TLR4 and food allergies.  TLR4 primarily senses lipopolysaccharides
(LPS) found in the outer membrane of Gram-negative bacteria which can
provoke immune responses, inflammation and have an endotoxic effect.  The
study finds that a disturbance of normal microflora, such as by
antibiotics, increases allergic responses.  Restoration of normal
microflora reduces allergic responses.  TLR4 signals provided by normal
microflora may be a factor in reducing food allergies.

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J Immunol. 2004 Jun 1;172(11):6978-87

Toll-like receptor 4 signaling by intestinal microbes influences
susceptibility to food allergy.

Bashir ME, Louie S, Shi HN, Nagler-Anderson C.

Mucosal Immunology Laboratory, Massachusetts General Hospital and Harvard
Medical School, Charlestown, MA 02129.

The mechanisms by which signaling by the innate immune system controls
susceptibility to allergy are poorly understood. In this report, we show
that intragastric administration of a food allergen with a mucosal adjuvant
induces allergen-specific IgE, elevated plasma histamine levels, and
anaphylactic symptoms in three different strains of mice lacking a
functional receptor for bacterial LPS (Toll-like receptor 4 (TLR4)), but
not in MHC-matched or congenic controls. Susceptibility to allergy
correlates with a Th2-biased cytokine response in both the mucosal
(mesenteric lymph node and Peyer's patch) and systemic (spleen) tissues of
TLR4-mutant or -deficient mice. TLR4-mutant mice are not inherently
impaired in their ability to regulate Th1 cytokine production because they
respond to stimulation via TLR9. Coadministration of CpG
oligodeoxynucleotides during sensitization of TLR4-mutant mice with
allergen plus CT abrogates anaphylactic symptoms and Ag-specific IgE, and
results in a Th1-polarized cytokine response. When the composition of the
bacterial flora is reduced and altered by antibiotic administration
(beginning at 2 wk of age), TLR4 wild-type mice become as susceptible to
the induction of allergy as their TLR4-mutant counterparts. Both allergen-
specific IgE and Th2 cytokine responses are reduced in antibiotic-treated
mice in which the flora has been allowed to repopulate. Taken together, our
results suggest that TLR4-dependent signals provided by the intestinal
commensal flora inhibit the development of allergic responses to food Ags.

PMID: 15153518 [PubMed - in process]

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