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

• Published in: Journal of leukocyte biology Vol. 66; no. 1; pp. 144 - 150
• Main Authors: Balish, Edward, Wagner, R. Doug, Vazquez‐Torres, Andres, Jones‐Carson, Jessica, Pierson, Carey, Warner, Thomas
• Format: Journal Article
• Language: English
• Published: United States Society for Leukocyte Biology 01.07.1999
• Subjects: Acute Disease; Animals; Antigens, CD - genetics; Antigens, CD - physiology; Candida albicans; Candidiasis - immunology; Candidiasis - microbiology; Candidiasis - pathology; chemokines; chemotaxis; Female; Indicators and Reagents; Injections, Intravenous; Intestinal Diseases - immunology; Intestinal Diseases - microbiology; Intestinal Diseases - pathology; Intestinal Mucosa - immunology; Intestinal Mucosa - microbiology; Intestinal Mucosa - pathology; Luminescent Measurements; Luminol; Male; Mice; Mice, Inbred BALB C; Mice, Knockout; neutrophils; Neutrophils - immunology; Receptors, Interleukin - genetics; Receptors, Interleukin - physiology; Receptors, Interleukin-8A
• ISSN: 0741-5400; 1938-3673
• DOI: 10.1002/jlb.66.1.144

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. J. Leukoc. Biol. 66: 144–150; 1999.