Inflammatory bowel disease pathogenesis

Gerhard R. Update in inflammatory bowel disease pathogenesis. Curr Opin Gastroenterol 2004 20 311-17. 

Hold, G. L., Smith, M., Grange, C., et al. (2014) Role of the gut microbiota in inflammatory bowel disease pathogenesis What have we learnt in the past 10 years World J Gastroenterol 7, 1192-1210. 

Linskens RK, Huijsdens XW, Savelkoul PH, Vandenbroucke-Grauls CM, Meuwissen SG The bacterial flora in inflammatory bowel disease Current insights in pathogenesis and the influence of antibiotics and probiotics. Scand J Gastroenterol 2001 36(suppl 234) 29-40. 

Although the pathogenesis of inflammatory bowel disease (IBD) remains unclear, increasing evidence suggests that the enteric microflora plays a central role in this process. The distal ileum and the colon are the areas with the highest bacterial concentrations and represent the sites of inflammation in IBD similarly pouchitis appears to be associated with bacterial overgrowth and dysbiosis. 

Inflammatory bowel disease (IBD) comprises two distinct disorders ulcerative colitis and Crohn s disease. The etiology and pathogenesis of these disorders remains unknown. For this reason, pharmacologic treatment of inflammatory bowel disorders often involves drugs that belong to different therapeutic classes and have different but nonspecific mechanisms of anti-inflammatory action. Drugs used in inflammatory bowel disease are chosen on the basis of disease severity, responsiveness, and drug... 

The pathogenesis of inflammatory bowel disease is still poorly understood. Immune mechanisms are probably involved, and potential antigens include intestinal bacteria and intestinal epithelium. Abnormalities in inflammatory mediators have also been described it has been suggested that an imbalance between proinflammatory and antiinflammatory cytokines may determine susceptibility, although the abnormalities observed could simply be secondary to the disease process. 

Day R, Forbes A. Heparin, cell adhesion, and pathogenesis of inflammatory bowel disease. Lancet 1999 354(9172) 62-5. 

MCP-1 and RANTES are thought to contribute to the recruitment and activation of leukocytes in mucosa from patients with inflammatory bowel disease, suggesting that these CKs play a role in the pathogenesis of mucosal inflammation. Furthermore, the expression of the MCP-1 gene in vessel-associated cells may indicate its involvement in mechanisms regulating the adhesion of blood monocytes to... 

As autacoids, bradykinin and kallidin increase vascular permeability, produce vasodilation, increase the synthesis of prostaglandins, and cause edema and pain. Extensive evidence exists that bradykinin and other kallidin substances contribute to the pathogenesis of the inflammatory response that occurs in acute and chronic diseases including allergic reactions, arthritis, asthma, sepsis, viral rhinitis, and inflammatory bowel diseases (see Figure 30). 

The role of both T and B lymphocytes in a variety of disease states beyond transplantation has become increasingly important in the past decade. This is especially true of those diseases frequently referred to as autoimmune in their etiology, such as rheumatoid arthritis, nephrotic syndrome, systemic lupus erythematosus, inflammatory bowel disease, and so on. In addition, several other major diseases are also known to have a component of T- or B-cell-mediated pathogenesis, for example, atopic dermatitis, psoriasis, and asthma. Until very recently, the mainstay of therapy for these diseases was the corticosteroids, which were often less than satisfactory in efficacy and often associated with undesirable side effects, especially in growing children and the elderly. Thus, the search for new agents with different mechanisms of action and which did not have the same adverse event profile as conventional corticosteroids led to the subsequent evaluation of drugs such as tacrolimus and sirolimus to treat several of these diseases. 

The reason for high variability in the outcomes of treating OA with CS is due to the variation in the chain length of the polymer used in these studies. While the high-quality, long-chain CS is more effective, the low-quality, short-chain CS has minimal effects on the pathogenesis of OA. Apart from its effects of improving OA, the anti-inflammatory effects of CS have led to improvement in conditions such as psoriasis and inflammatory bowel disease. These effects... 

Geier, M.S., Butler, R.N., and Howarth, G.S. (2007) Inflammatory bowel disease Current insights into pathogenesis and new therapeutic options probiotics, prebiotics and synbiotics. International Journal of Food Microbiology, 115, 1-11. 

Inflammatory bowel disease (IBD), alongside Crohn s disease (CD) and ulcerative colitis are characterized by the inflammation of the gastrointestinal tract. The etiology of IBD is induced by a combination of factors that contributes to this pathogenesis. 

PPARa), an orphan nuclear receptor that acts as a transcription factor to induce the expression of enzymes involved in fatty acid oxidation (Devchand et al, 1996). Abnormal LTB4 production has been implicated in the pathogenesis of inflammatory bowel disease, psoriasis, rheumatoid arthritis, and gout. 

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