Mucosal and systemic candidiasis in IL-8Rh-/- BALB c mice

Germ-free BALB/c mice, genetically engineered to be deficient for interleukin-8 (IL-8) receptor homolog (IL-8Rh(-/-)), were more susceptible to gastric candidiasis after oral challenge and to acute systemic candidiasis after intravenous challenge than IL-8Rh(+/+) controls. In comparison to IL-8Rh(+/+) mice, the IL-8Rh(-/-) mice had slower influx of polymorphonuclear neutrophils (PMN) into Candida albicans-infected tissues and a lo,ver percentage of PMN in peritoneal exudate cells (PEC) elicited with heat-killed C. albicans. PEC front IL-8Rh(-/)- mice exhibited less luminol-dependent chemiluminescence in response to C, albicans and did not kill C. albicans hyphae as well as PEC from IL-8Rh(+/+) mice. C. albicans-colonized IL-8Rh(-/-) mice showed no histological evidence of systemic candidiasis. These results suggest a role for the IL-8Rh iu murine resistance to gastric and acute systemic candidiasis, but not in resistance to systemic candidiasis of endogenous origin.