The immunopathology of inflammatory bowel disease consists of a sequen
ce of immunological steps that begin with initial antigen processing e
vents. A major focus has recently been placed on bacterial cell wall p
roducts (peptidoglycans, formyl-methionyl-leucyl phenylalanine, lipopo
lysaccharides). These products nonspecifically induce an intense activ
ation of macrophages, granulocytes, ana lymphocytes. Currently, theref
ore, the working hypothesis is that in inflammatory bowel disease, ubi
quitous and common bacterial cell wall products capable of initiating
an inflammatory immune response, in a genetically predisposed individu
al, activate a sequence of immunologic processes that are not appropri
ately downregulated. Initiating events then lead to macrophage activat
ion, with the resultant production of large amounts of IL1, 116, 118,
and TNF-alpha. Subsequent cell-mediated immunologic events involve the
mucosal immune system, and lead to the chronic intestinal destruction
associated with inflammatory bowel disease.