
I'm not holding my breath.

Tex
Moderators: Rosie, Stanz, Jean, CAMary, moremuscle, JFR, Dee, xet, Peggy, Matthew, Gabes-Apg, grannyh, Gloria, Mars, starfire, Polly, Joefnh
Viruses Can Turn Harmless E. Coli DangerousProfessor Jon Rhodes, from the University’s School of Clinical Sciences, explains: “Mycobacterium paratuberculosis has been found within Crohn’s disease tissue but there has been much controversy concerning its role in the disease. We have now shown that these Mycobacteria release a complex molecule containing a sugar, called mannose. This molecule prevents a type of white blood cells, called macrophages, from killing internalised E.Coli.”
Scientists have previously shown that people with Crohn’s disease have increased numbers of a ‘sticky’ type of E.coli and weakened ability to fight off intestinal bacteria. The suppressive effect of the Mycobacterial molecule on this type of white blood cell suggests it is a likely mechanism for weakening the body’s defence against the bacteria.
Professor Rhodes added: "We also found that this bacterium is a likely trigger for a circulating antibody protein (ASCA) that is found in about two thirds of patients with Crohn's disease, suggesting that these people may have been infected by the Mycobacterium."
http://bmb.oxfordjournals.org/cgi/reprint/88/1/95.pdfIntroduction/background: Inflammatory bowel disease (IBD) results from
complex interactions between: host genome, immune system, mucosa, bacteria,
and environment.
Sources of data: Review of PubMed database using search terms ‘bacteria and
inflammatory bowel disease’ and ‘genetics and inflammatory bowel disease’.
PubMed ‘related reference’ feature and references from retrieved articles were
examined.
Areas of agreement: IBD results from interaction between the microbiota of the
gut and the immune system. Key gene defects associated with IBD are involved
in bacterial recognition and processing. The environment at least modifies and
may determine pathogenesis.
Areas of controversy: It has been disputed whether the primary defect in IBD is
immunological or bacterial, and which bacteria are key.
Growing points/areas for research: ‘M cells’, the specialized epithelial cells that
overlie Peyer’s patches, are a major interface between gut bacteria and the
immune system. Improved understanding is needed of the bacteria involved in
IBD pathogenesis, their genotypes and phenotypes, their portal of entry and
their mechanism for escaping attack from the immune system. Bacterial ligands
involved in bacteria–epithelial adhesion are emerging, and molecular
techniques are rapidly increasing our knowledge of the human intestinal
microbiota.