Interleukin I (IL-1) may be a key mediator of inflammation and tissue damage in inflammatory bowel disease (IBD). In rabbits with immune complex-induced colitis, IL-la and (3 mRNA levels were detectable at 4 h, peaked at 12 but were absent at 96 h after the induction of colitis. Colonic IL-1 tissue levels were measured by specific radioimmunoassays. IL-la was significantly elevated at 4 h (9.4±1.5 ng/g colon), progressively increased at 48 h (31±5.8 ng/g) and then decreased by 96 h (11.5±3.4 ng/g). IL-lft levels were 2.0±0.5 ng/g colon at 4 h, 5.0±1.6 ng/g at 48 h and undetectable by 96 h. By comparison, colonic levels of PGE2 and LTB4 were unchanged during the first 12 h and did not become elevated until 24 h. IL-la levels were highly correlated with inflammation (r = 0.885, P < 0.0001), edema (r = 0.789, P < 0.0001) and necrosis (r = 0.752, P < 0.0005). Treatment with a specific IL-1 receptor antagonist (IL-Ira) before and during the first 33 h after the administration of immune complexes markedly reduced inflammatory cell infiltration index (from 3.2±0.4 to 1.4±0.3, P < 0.02), edema (from 2.2±0.4 to 0.6±0.3, P < 0.01) and necrosis (from 43±10% to 6.6±3.2%, P < 0.03) compared to vehicle-matched colitis animals. These studies demonstrate

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Interleukin-1 (IL-1) is a polypeptide cytokine that mediates many physiological responses to infection and inflammation and is a growth factor for certain mammalian cells. Virulent and avirulent clinical isolates of Escherichia coli were grown in culture media in the presence of human IL-1. IL-1 beta, but not tumor necrosis factor or IL-4, enhanced the growth of virulent, but not avirulent, E. coli. This enhancement was blocked by the IL-1 receptor antagonist (IL-1ra). Radiolabeled IL-1 bound to virulent but not avirulent E. coli in a specific and saturable fashion; IL-1ra inhibited this binding. Thus, human IL-1 may recognize a functional IL-1-like receptor structure on virulent E. coli and may be a virulence factor for bacterial pathogenicity.

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