Abstract
Crohn's disease (CD) is caused by a trigger, almost certainly enteric infection by one of a multitude of organisms that allows faeces access to the tissues, at which stage the response of individuals predisposed to CD is abnormal. In CD the failure of acute inflammation results in the failure to recruit neutrophils to the inflammatory site, as a consequence of which the clearance of bacteria from the tissues is defective. The retained faecal products result in the characteristic chronic granulomatous inflammation and adaptive immune response. Impaired of digestion of bacteria and fungi by CGD neutrophils can result in a similar pathological and clinical picture. The neutrophils in CD are normal and their inadequate accumulation at sites of inflammation generally results from diminished secretion of proinflammatory cytokines by macrophages consequent upon disordered vesicle trafficking.
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