Figure 1 Pathogenesis of Inflammatory Bowel Disease. Normal epithelium, with its highly evolved tight junctions and products of goblet-cell populations, most notably trefoil peptides and mucin glycoproteins, provides an effective barrier against luminal agents. The integrity of the barrier may be compromised by genetic variations in key molecular determinants, a diminished reparative response to injury, or exogenous agents, such as nonsteroidal antiinflammatory drugs. Chronic, recurrent intestinal inflammation appears to result from stimulation of the mucosal immune system by products of commensal bacteria in the lumen. Antigens from dietary sources may also contribute. Stimulation may occur as a result of the penetration of bacterial products through the mucosal barrier, leading to their direct interaction with immune cells, especially dendritic cells and lymphocyte populations, to promote a classic adaptive immune response.

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Alternatively, bacterial products may stimulate the surface epithelium, possibly through receptors that are components of the innate immune-response system; the epithelium can, in turn, produce cytokines and chemokines that recruit and activate mucosal immune cells. Activation of classic antigen-presenting cells, such as dendritic cells, or direct stimulation through pattern-recognition receptors promotes the differentiation of type 1 helper T cells (Th1) in patients with Crohn's disease (shown here) or, possibly, atypical type 2 helper T cells in patients with ulcerative colitis. The stereotypical products of Th1 promote a self-sustaining cycle of activation with macrophages. In addition to producing the key cytokines that stimulate Th1 (interleukin-12, interleukin-18, and macrophage migration inhibitor factor), macrophages produce a mix of inflammatory cytokines, including interleukin-1, interleukin-6, and most notably tumor necrosis factor, which target a broad variety of other types of cells. The latter include endothelial cells, which then facilitate the recruitment of leukocytes to the mucosa from the vascular space, as well as fibroblasts and epithelium, modulating their functional properties.

Most important, these functions may be altered either by genetically determined variants, as exemplified by germ-line mutations in the gene encoding NOD2, the product of the IBD1 locus, in some patients with Crohn's disease, or by environmental factors. Figure 2 Common Cellular Pathways of Activation in Inflammatory Bowel Disease. Activation of the protean transcriptional regulatory factor nuclear factor-κB (NF-κB) is a common pathway central to cell activation and the production of diverse inflammatory mediators, including a variety of cytokines and chemokines. It also modulates resistance to programmed cell death (apoptosis). Several inflammatory factors implicated in inflammatory bowel disease activate NF-κB by eventually stimulating an intermediate kinase such as NF-κB–inducing kinase (NIK) or mitogen-activated protein kinase kinase 1 or 3 (MEKK1 or MEKK3) or by binding to receptor-interacting protein 2.

Arasu Kannada Movie Preethi Preethi Songs Free Download. These lead to phosphorylation of the inhibitor of κB kinase (IKK) and subsequent dissociation of NF-κB (itself a dimer). NF-κB then travels to the nucleus, where it can effect gene transcription. The phosphorylated constituents are subject to degradation by proteosomes after ubiquitination. The spectrum of mediators that activate this pathway includes inflammatory cytokines such as interleukin-1 and tumor necrosis factor (TNF), which bind to their respective cell-surface receptors, as well as microbial products such as lipopolysaccharide, which bind to cell-surface receptors that are members of the toll-like receptor family of pattern-recognition receptors. The pathway is also activated by NOD2 (also referred to as CARD 15), an intracytoplasmic receptor that is activated by the entry, through mechanisms yet to be defined, of bacterial lipopolysaccharide into the cytoplasm.