| Inflammatory Bowel Disease (IBD) happens increasingly year after year in China. But its causes and pathogenesis are still not clear yet. Since several years, the ways for treatment have not still been made any obvious progress and the healing effects are not satisfactory. However, recent researches on cytokine and chemokine, especially on NF-kappaB and Toll recipients, has gradually revealed pathogenesis of IBD and already or will provide theoretical foundations for developing new ways for treatment.IBD owns a complex process of chronic inflammation. Recent researches has indicated that probably metabolite of intestinal bacteria act on host susceptible to gene susceptibility, which makes IBD build up immune answer . These three parties play very important role of cooperation at beginning and sustainable development of the inflammation. The researches on environment factors mainly focus on intestinal infection. As everyone knows, the disease is not caused by pure bacteria or virus infections. Researches on effects caused by sub-tubercle branch bacilli to the disease are still in ascendant. Environment changes in intestine cavity, specially changes of bacterium group, is vital to happening of bowel inflammation probably through antigen stimulation, metabolism of epithelial cells of intestine and penetrability to intestine wall and influence to conglutinating immune system. In researches of genetic etiology, people have defined several chain scopes in which at the place of IBD1 of 16q12 is existed that NOD2 is obviously related to susceptibility of CD. Mutation of NOD2 causes immune activation andabnormity of immune modulation mechanism and leads to damages to cells and organization. The investigations in Genetic epidemiology have proved that the mutation is probable the main cause of 30% of CD and changes genetic characteristics of sub-group CD. This great discovery has epoch-making significance, which makes genetic etiology completely affirmed and will integrate changes of genetics and abnormity of immune reaction of contagious genes. The discovery can completely explain attack of sub-group CD.Together with trefoil peptides and mucin glycoproteins excreted by cupped cells, normal intestine epithelium walls separate a lot of antigens in the intestine cavity from immune cells of original membrane. However integrality of intestinal mucous membrane screen will probably get weak, caused by mutation of determinative groups of key gene molecules. Metabolins from bacteria group in intestine cavity penetrate intestinal mucous membrane screen and cause immune reaction of immune cells in original membrane. Submissive cells of antigen absorb antigen in intestinal cavity for processing and connect a small segment of antigen to glycoproteins on cell surface. After that, they cooperate with T recipient to make various CD4+T cells produce cell genes. After activation of T cells, they will consist of a self-driven feedback circulation together with macrophages, which makes macrophages produce not only IL-12, IL-18 but also a series of cells like TNF, IL-1 and IL-6.NF-kappaB belongs to a kind of highly-conservative nuclear factor in evolutionism. It exists in various organizations and can have diathetic integration with kappaB transcriptional serial sequence in initiators and enhancers of many cell genes. It also involves many genetic modulations in physiology and pathology process such as in transcriptional modulation and resistance to programmed cell death (apoptosis) in many immue inflammatory reactions and in adhering and displacing of tumor cells. In IBD, NF-kappaB is activated by an active agent to adjust sendor production of inflammation and leads to damages of IBD inflammatory mucous membrane. Therefore, NF-kappaB is acting as a hub in the process of physiology and pathology. NF-kappaB is modulated by 1KB in its cell liquid. In resting cell cytoplasm, NF-kappaB integrates 1KB to compose an inactivetri-polymer. Simulative genes in up-stream like TNF-a, IL-lp, oxidizer and lipopolysaccharide, integrate with rela...
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