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Introduction

Intestinal epithelial cells serve as a barrier between the body and viruses, bacteria, and parasites present in the intestinal lumen. Rather than being a passive barrier, the intes­tinal epithelium is an active participant in the mucosal immune response through antigen processing and presentation, secretion of cytokines, and recruitment of inflammatory cells in response to pathogens and their products.

The gastrointestinal-associated lymphoid tissue (GALT) is the largest and most complex immunological organ of the body and must be capable of mounting a protective immune response to pathogens, while maintaining tolerance to harmless environmental antigens such as commensal bacteria and food. The breakdown of this tolerance is a key factor in the development of chronic intestinal inflammation.

In the dog and cat, inflammatory bowel disease (IBD) is the collective term for a group of chronic enteropathies characterized by persistent or recurrent gastrointestinal signs and inflammation of the gastrointesti­nal tract (Simpson and Jergens 2011). The specific steps that lead to IBD and the basis for phenotypic variation and unpredictable responses to treatment are not known. The breakdown of immunologic tolerance to luminal antigens (bacteria and dietary com­ponents) is thought to be critical, perhaps resulting from disruption of the mucosal barrier, dysregulation of the immune system, or disturbances in the intestinal microflora (Burgener et al. 2008; Dandrieux, Bornand, and, Burgener 2008; Xenoulis, Palculict, and Allenspach 2008). Until recently, histiocytic ulcerative colitis (HUC) was also considered a special form of IBD of unknown etiology, however, it has now been identified as being caused by an adherent and invasive pheno­type of E.coli (Simpson et al. 2006). These findings elucidated the success of the antibi­otic therapy for HUC, which included enro- floxacin (Hostutler et al. 2004).

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Source: Gram W.D., Milner R.J., Lobetti R. (eds.). Chronic Disease Management for Small Animals. Wiley,2018. — 357 p.. 2018

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