Abstract
BackgroundThere is increasing evidence that bacterial infection of the intestinal mucosa may contribute to the pathogenesis of inflammatory bowel diseases (IBD). In pigs, an obligate intracellular bacterium, Lawsonia intracellularis (LI), was shown to cause proliferative enteropathy (PE) of which some forms display histological and clinical similarities to human IBD. Since LI-similar Desulfovibrio spp. may infect human cells, we hypothesized that LI might be associated with the development of human IBD.ResultsIn human intestinal tissue samples, PCR using LLG, 50SL27, LSA and strictly LI-specific 16SII primers, yielded either no amplicons or products with weak homology to human genomic sequences. Sequencing of these amplicons revealed no specificity for LI. However, amplification of DNA with less specific 16SI primers resulted in products bearing homology to certain Streptococcus species. These 16SI-amplified products were present in healthy and diseased specimens, without obvious prevalence.ConclusionLI is not associated with the pathogenesis of UC or CD. Whether an immunologic response to commensal bacteria such as streptococci may contribute to the chronic inflammatory condition in IBD, remained to be determined.
Highlights
There is increasing evidence that bacterial infection of the intestinal mucosa may contribute to the pathogenesis of inflammatory bowel diseases (IBD)
Inflammatory bowel diseases (IBD) comprises primarily Crohn's disease (CD) and ulcerative colitis (UC) which are characterized by recurrent inflammatory attacks associated with tissue destruction [1,2]
Mycobacterium paratuberculosis has been found in tissue and blood samples of CD patients, though the question whether mucosal dysregulation leads to infection or vice versa remains unanswered [4,9,10]
Summary
There is increasing evidence that bacterial infection of the intestinal mucosa may contribute to the pathogenesis of inflammatory bowel diseases (IBD). Mycobacterium paratuberculosis has been found in tissue and blood samples of CD patients, though the question whether mucosal dysregulation leads to infection or vice versa remains unanswered [4,9,10]. It is unclear whether this bacterium is an etiologic factor or is detected solely by coincidence, and has no influence on the course of the disease. In UC, there is evidence for a cross-talk between commensal bacteria and the mucosal immune system while the exact role of these bacteria has to be further elucidated [5]
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