Host defenses against disseminated candidiasis are impaired in intercellular adhesion molecule 1-deficient mice.
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.
Davis
S L
SL
Department of Pediatrics, Baylor College of Medicine, Houston, Texas, USA.
Hawkins
E P
EP
Mason
E O
EO
Smith
C W
CW
Kaplan
S L
SL
D000818:Animals; D001921:Brain / Q000382:microbiology / Q000473:pathology; D002177:Candidiasis / Q000276:immunology* / Q000401:mortality / Q000473:pathology; D016469:Fungemia / Q000276:immunology / Q000401:mortality / Q000473:pathology; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics*; D007668:Kidney / Q000382:microbiology / Q000473:pathology; D051379:Mice; D008817:Mice, Mutant Strains; D009504:Neutrophils / Q000276:immunology; D010586:Phagocytes / Q000276:immunology; D015431:Weight Loss
D018799:Intercellular Adhesion Molecule-1