Search
Close
Search
Advanced Search
Search Menu
AI Discovery Assistant

Abstract

BackgroundInterleukin (IL)–1α and IL-1β are protective proinflammatory cytokines involved in host defense against Candida albicans. It is, however, unknown whether they provide protection through similar mechanisms. We investigated the effect of endogenous IL-1α and IL-1β on disseminated C. albicans infection

MethodsMice deficient in the genes encoding IL-1α (IL-1α−/−), IL-1β (IL-1β−/−), or both molecules (IL-1α−/−β−/−) were used. Survival and C. albicans outgrowth in the kidneys was assessed after intravenous injection of C. albicans

ResultsBoth mortality and C. albicans outgrowth in the kidneys were significantly increased in IL-1α−/− and IL-1β−/− mice, compared with those in control mice, with the IL-1α−/−β−/− mice being most susceptible to disseminated candidiasis. The host defense mechanisms triggered by IL-1α and IL-1β differed from one another. IL-1β−/− mice showed decreased recruitment of granulocytes in response to an intraperitoneal C. albicans challenge, and generation of superoxide production was diminished in IL-1β−/− granulocytes. IL-1α−/− mice had a reduced capacity to damage C. albicans pseudohyphae. Protective type 1 responses were deficient in both IL-1α−/− and IL-1β−/− mice, as assessed by production of interferon-γ by splenocytes in response to heat-killed C. albicans

ConclusionAlthough IL-1α and IL-1β have differential effects on the various arms of host defense, both cytokines are essential for mounting a protective host response against invasive C. albicans infection

© 2006 by the Infectious Diseases Society of America
Topic:
Issue Section:
Major Article
You do not currently have access to this article.
Download all slides