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This is exciting!!!

I have in the recent past been advocating on this Celiac List that celiac
disease research take a look at the possibility that bacteria play a role
in the pathogenesis of celiac disease (see the Celiac List archives).  To
that end, I contributed an article entitled, "Are Commensal Bacteria with a
taste for Gluten the Missing Link in the Pathogenesis of Celiac Disease?"
which appears in the current Spring 2004 edition of Scott
Adams' "Celiac.com's Guide to A Scott-Free Life Without Gluten".  That
article proposes that the immune system may become intolerant to gluten via
an unknown species of pathogenic bacteria which is able to internalize
gluten peptides.  The result is that when dendritic cells (antigen
presenting cells) sample the pathogenic bacteria and break it down into
peptides for presentation to naive T cells, the internalized gluten
peptides are mixed with the bacteria's own native peptides.  The immune
system would not be able to distinguish internalized gluten peptides from
the pathogenic bacteria peptides.  When the dendritic cell presents these
internalized gluten peptides to a T cell, the T cell would receive signals
which tell the T cell that the internalized gluten peptides are from a
pathogenic bacteria.  Hence the immune system would learn to respond to
gluten peptides as though a pathogenic bacteria were present, resulting in
gluten intolerance.  (This is discussed in much greater detail in my
article.)

Now for the first time, researchers have found a bacteria that appears to
be associated with  celiac disease.  I strongly urge that scientists look
for gluten peptides within these bacteria and confirm my theory.  A
techique called autoradiography can be used to create images of
radionuclide-labelled gluten peptides internalized by bacteria on x-ray
emulsion film viewed under electron microscope.  If this theory is
verified, then a possible cure for celiac disease and restoration of gluten
tolerance might exist by eliminating these bacteria from the gut.

I certainly hope the topic of bacteria and celiac disease is discussed at
the NIH Celiac Disease Consensus Conference in June.

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Am J Gastroenterol. 2004 May;99(5):905-906

A Role for Bacteria in Celiac Disease?

Ludvig M. Sollid, M.D., Gary M. Gray, M.D.

The finding of rod-shaped bacteria attached to the small intestinal
epithelium of some untreated and treated celiac-disease patients, but not
to the epithelium of healthy controls, ignites the notion that bacteria may
be involved in the pathogenesis of celiac disease. This editorial discusses
this possibility in relation to the current understanding of the molecular
basis of this disorder.

PMID: 15128358 [PubMed]

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Am J Gastroenterol. 2004 May;99(5):894-904

Presence of bacteria and innate immunity of intestinal epithelium in
childhood celiac disease.

Forsberg G, Fahlgren A, Horstedt P, Hammarstrom S, Hernell O, Hammarstrom
ML.

Department of Clinical Microbiology and Immunology; Department of Clinical
Sciences and Pediatrics; and Department of Medical Biosciences, Pathology,
Umea University, Umea, Sweden.

OBJECTIVES: Exposure to gliadin and related prolamins and appropriate HLA-
DQ haplotype are necessary but not sufficient for contracting celiac
disease (CD). Aberrant innate immune reactions could be contributing risk
factors. Therefore, jejunal biopsies were screened for bacteria and the
innate immune status of the epithelium investigated. METHODS: Children with
untreated, treated, challenged CD, and controls were analyzed. Bacteria
were identified by scanning electron microscopy. Glycocalyx composition and
mucin and antimicrobial peptide production were studied by quantitative RT-
PCR, antibody and lectin immunohistochemistry. RESULTS: Rod-shaped bacteria
were frequently associated with the mucosa of CD patients, with both active
and inactive disease, but not with controls. The lectin Ulex europaeus
agglutinin I (UEAI) stained goblet cells in the mucosa of all CD patients
but not of controls. The lectin peanut agglutinin (PNA) stained glycocalyx
of controls but not of CD patients. mRNA levels of mucin-2 (MUC2), alpha-
defensins HD-5 and HD-6, and lysozyme were significantly increased in
active CD and returned to normal in treated CD. Their expression levels
correlated to the interferon-gamma mRNA levels in intraepithelial
lymphocytes. MUC2, HD-5, and lysozyme proteins were seen in absorptive
epithelial cells. beta-defensins hBD-1 and hBD-2, carcinoembryonic antigen
(CEA), CEA cell adhesion molecule-1a (CEACAM1a), and MUC3 were not
affected. CONCLUSIONS: Unique carbohydrate structures of the
glycocalyx/mucous layer are likely discriminating features of CD patients.
These glycosylation differences could facilitate bacterial adhesion.
Ectopic production of MUC2, HD-5, and lysozyme in active CD is compatible
with goblet and Paneth cell metaplasia induced by high interferon-gamma
production by intraepithelial lymphocytes.

PMID: 15128357 [PubMed]

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