Eosinophilia is attenuated in experimental colitis induced in IL-5 deficient mice.

Abstract

Tissue eosinophilia is a feature of idiopathic inflammatory bowel disease and other forms of colonic inflammation but it is not clear whether the role of eosinophils in the disease process is to contribute to tissue damage. Interleukin 5 (IL-5) stimulates production and activation of eosinophils in vitro and enhances immunoglobulin A (IgA) production. As very little is known about the function of IL-5 in the colon, the aim of this study was to assess its role in colonic inflammation. IL-5 deficient mice were studied using the dextran sulphate sodium (DSS)-induced colitis model and the results compared to a congenic IL-5+/+ strain. The absence of IL-5 resulted in reduction of tissue eosinophilia (P < 0.0001) but was not reflected in differences in the severity of the disease (P > 0.5) or in the extent of tissue damage in this model of colitis. Numbers of immunoglobulin-containing cells in IL-5 deficient mice were similar to those in the IL-5+ mice. We conclude that the main role of IL-5 in DSS-induced colonic inflammation is to attract a population of eosinophils which do not appear to contribute significantly to the initiation or development of tissue damage in this model of colitis.