ABSTRACT
CONTENTS Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 375 Bacteria and IBD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 376 Bacterial Communities in the Gut . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 377 The Gut Microbiota in IBD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 380 Prebiotics and Gut Microbiota . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 381 Prebiotics in Experimental Models of IBD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 382 Clinical Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 386 Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 389 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 389
The inflammatory bowel diseases (IBD), Crohn’s disease, ulcerative colitis, and pouchitis, are chronic conditions of unknown etiology characterized by persistent mucosal inflammation at different levels of the gastrointestinal tract. Typically, thesediseases exhibit undulatingactivitywithboutsofuncontrolled, chronic mucosal inflammation, followed by remodeling processes that occur during periods of remission [1]. The precise etiologies of these chronic inflammatory conditions remain to be elucidated and, therefore, available medical therapies can only control, to some extent, the eruptions of disease activity, but fail completely regarding eradication or permanent cure of such diseases. However, pathophysiological mechanisms that lead to mucosal inflammatory lesions have been unveiled at least in part during the past few years. These mechanisms result from complex interactions of environmental, genetic and immunoregulatory factors. Two broad hypotheses have arisen regarding the fundamental nature of the pathogenesis of IBD [2]. The first argues that primary dysregulation of the mucosal immune system leads to excessive immunological responses to normal microbiota. The second suggests that changes in the composition of gut microbiota
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and/orderangedepithelial barrier function elicit pathological responses from the normal mucosal immune system (Figure 18.1). In either case, abnormal communication between gut microbial communities and the mucosal immune system is incriminated as the core defect leading to IBD in genetically susceptible individuals. Within the gastrointestinal tract, the inflammatory capacity of commensal
bacteria is varied. Some resident bacteria are proinflammatory, whereas others attenuate inflammatory responses [3-5]. Prebiotics such as inulin and oligofructose can improve the microbial balance in the human intestinal ecosystem by increasing the number and activity of bacteria associated with health benefits [6]. This chapter reviews experimental and clinical evidence supporting the use of prebiotics for the prevention and control of IBD.
