| First Author | Balish E | Year | 1999 |
| Journal | J Leukoc Biol | Volume | 66 |
| Issue | 1 | Pages | 144-50 |
| PubMed ID | 10411002 | Mgi Jnum | J:56315 |
| Mgi Id | MGI:1340795 | Doi | 10.1002/jlb.66.1.144 |
| Citation | Balish E, et al. (1999) Mucosal and systemic candidiasis in IL-8Rh-/- BALB/c mice. J Leukoc Biol 66(1):144-50 |
| abstractText | 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. |
