Conclusions

In IBD, the state of activation of the intestinal immune system and mucosal inflammatory pathways are markedly upregulated. The mechanisms that normally downregulate the immunologic and inflammatory protective processes, once the inflammatory stimulus has been cleared, appear to be deficient or are suboptimal. Knockout mice that do not express IL-10, a cytokine that normally downregulates immune responses, have a number of features of inflammatory bowel disease. It is possible that changes in immunological responsiveness in IBD are genetically controlled. A critical area of investigation is the elucidation of the genetic factors that predispose certain individuals either to having a heightened immune and inflammatory response or an inability to downregulate ongoing chronic immunologic and inflammatory events.

See also: Acute inflammatory reaction; Adhesion molecules; Antigen, entry into the body; Chemokines; Chemotaxis; Cytokines; Endotoxin

(lipopolysaccharide (LPS)); Macrophage activation; Monocyte chemotactic protein 1 (MCP-1); Mucosal immunity; Prostaglandins.

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