| First Author | Davis SL | Year | 1996 |
| Journal | J Infect Dis | Volume | 174 |
| Issue | 2 | Pages | 435-9 |
| PubMed ID | 8699084 | Mgi Jnum | J:34394 |
| Mgi Id | MGI:81854 | Doi | 10.1093/infdis/174.2.435 |
| Citation | Davis SL, et al. (1996) Host defenses against disseminated candidiasis are impaired in intercellular adhesion molecule 1-deficient mice. J Infect Dis 174(2):435-9 |
| abstractText | Genetically engineered mice, which lack normal expression of intercellular adhesion molecule 1 (ICAM-1), were used to study the role of ICAM-1 in the host defense against disseminated candidiasis. The responses of ICAM-1-deficient mice and normal wild type mice were compared following an intravenous challenge with Candida albicans. ICAM-1-deficient mice lost more weight (P < .001) and had a significantly higher mortality (P < .001). Quantitative cultures revealed a greater tissue fungal burden in ICAM-1-deficient mice compared with normal mice, in both the kidney (P < .001) and the brain (P = .007). Extensive inflammation, composed primarily of histiocytes admixed with lymphocytes and occasional neutrophils, was present in the renal tissue of ICAM-1-deficient mice; this contrasted with a more localized and predominantly neutrophilic infiltrate in normal mice. This work suggests that the loss of ICAM-1 significantly impairs host defense against C. albicans, by impairing either neutrophil migration or phagocyte activation or both. |
