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J Leukoc Biol. 1999 Jul;66(1):144-50.

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

Author information

1
Department of Surgery, University of Wisconsin Medical School, Madison 53706-1532, USA. balish@surgery.wisc.edu

Abstract

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 lower percentage of PMN in peritoneal exudate cells (PEC) elicited with heat-killed C. albicans. PEC from 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 in murine resistance to gastric and acute systemic candidiasis, but not in resistance to systemic candidiasis of endogenous origin.

PMID:
10411002
DOI:
10.1002/jlb.66.1.144
[Indexed for MEDLINE]

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