Human inflammatory bowel disease does not associate with Lawsonia intracellularis infection

In 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.LI 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.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]. The etiology of these diseases is multifactorial and genetic or infectious factors have been postulated to be part of the formation of the chronically inflammatory condition [3-5]. Besides some contributing genetic factors such as NOD2/CARD15 variants in CD patients, there seems to be an impairment in the intestinal mucosal barrier function leading to defective immunoregulation [6-8]. Furthermore, there is increasing evidence that bacterial infection of the intestinal mucosa may be involved in its pathogenesis [5]. In particular, 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 also unclear whether this bacterium is an etiologic factor or is detected solely by coincidence, and thus 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 also has to be further elucidated [5].The obligate in