title: Role of intercellular adhesion molecule 1 in acute lung injury induced by candidemia.
abstract: Candidemia, a complication often affecting immunocompromised patients, is a common cause of acute lung injury. Yeast-phase Candida albicans has been shown to express a protein that is antigenically and structurally related to Mac-1. C. albicans is reported to stimulate intercellular adhesion molecule 1 (ICAM-1) expression on endothelial cells. In this study, the authors examined the role of ICAM-1 in acute lung injury induced by candidemia. The authors cultured rat pulmonary artery endothelial cells (RPAEC) and investigated the effect of anti-ICAM-1 antibodies on adhesion of C. albicans to RPAEC. In addition, the authors administered anti-ICAM-1 antibodies to rats to examine the effect of the antibodies on experimentally induced candidemia. Survival rates, lung wet-to-dry (W/D) weight ratios, bronchoalveolar lavage (BAL) fluid, histopathological findings, and colony-forming units (CFUs) of lung C. albicans were examined. The adherence of C. albicans to RPAEC was significantly decreased by anti-ICAM-1 antibodies. Anti-ICAM-1 antibodies significantly increased survival, decreased lung W/D weight ratios, decreased neutrophil counts in the BAL fluid, reduced microscopic lung injury, and decreased the quantity of lung C. albicans. These results indicate that ICAM-1 plays a role in adherence of C. albicans to pulmonary vascular endothelial cells, which likely leads to invasion of lung tissue by the organism.
authors.affiliation: Second Department of Medicine, Kyoto Prefectural University of Medicine, Japan. iycyay@ec.mbn.or.jp
authors.forename: I
authors.initials: I
authors.lastname: Yokomura
authors.forename: Y
authors.initials: Y
authors.lastname: Iwasaki
authors.forename: K
authors.initials: K
authors.lastname: Nagata
authors.forename: M
authors.initials: M
authors.lastname: Nakanishi
authors.forename: A
authors.initials: A
authors.lastname: Natsuhara
authors.forename: H
authors.initials: H
authors.lastname: Harada
authors.forename: Y
authors.initials: Y
authors.lastname: Kubota
authors.forename: M
authors.initials: M
authors.lastname: Ueda
authors.forename: T
authors.initials: T
authors.lastname: Inaba
authors.forename: M
authors.initials: M
authors.lastname: Nakagawa
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000008:administration & dosage / Q000494:pharmacology; D001422:Bacterial Adhesion / Q000187:drug effects; D002176:Candida albicans / Q000166:cytology / Q000187:drug effects; D002177:Candidiasis / Q000150:complications* / Q000188:drug therapy / Q000473:pathology; D018929:Cell Culture Techniques; D004730:Endothelium, Vascular / Q000166:cytology; D016469:Fungemia / Q000150:complications / Q000188:drug therapy; D018799:Intercellular Adhesion Molecule-1 / Q000276:immunology / Q000502:physiology*; D008297:Male; D023421:Models, Animal; D009929:Organ Size / Q000187:drug effects; D011651:Pulmonary Artery / Q000166:cytology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012128:Respiratory Distress Syndrome / Q000188:drug therapy / Q000382:microbiology* / Q000473:pathology; D015996:Survival Rate
chemical_list: D000911:Antibodies, Monoclonal; D018799:Intercellular Adhesion Molecule-1