Host defenses against disseminated candidiasis are impaired in intercellular adhesion molecule 1-deficient mice

Susan L. Davis, Edith P. Hawkins, Edward Mason, C. Wayne Smith, Sheldon Kaplan

Research output: Contribution to journalArticle

31 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)435-439
Number of pages5
JournalJournal of Infectious Diseases
Volume174
Issue number2
DOIs
StatePublished - 1996

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases

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