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

被引:39
作者
Balish, E
Wagner, RD
Vazquez-Torres, A
Jones-Carson, J
Pierson, C
Warner, T
机构
[1] Univ Wisconsin, Sch Med, Dept Surg, Madison, WI 53706 USA
[2] Univ Wisconsin, Sch Med, Dept Med Microbiol & Immunol, Madison, WI 53706 USA
[3] Univ Wisconsin, Sch Med, Dept Surg Pathol, Madison, WI 53706 USA
[4] Natl Ctr Toxicol Res, Div Microbiol, Jefferson, AR 72079 USA
[5] Univ Colorado, Hlth Sci Ctr, Div Infect Dis, Denver, CO USA
[6] Natl Jewish Med & Res Ctr, Dept Med, Denver, CO USA
关键词
chemokines; Candida albicans; neutrophils; chemotaxis;
D O I
10.1002/jlb.66.1.144
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:144 / 150
页数:7
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