title: Expression of adhesion molecules in lungs of mice infected with Paracoccidioides brasiliensis conidia.
abstract: In infected tissues, leukocyte recruitment is mediated by interactions between adhesion molecules, expressed on activated vascular endothelial cells, and ligands present on circulating cells. We evaluated the inflammatory response and the expression of cellular adhesion molecules (ICAM-1, VCAM-1, CD18, LFA-1 and Mac-1) in lungs of BALB/c mice infected with Paracoccidioides brasiliensis conidia. When compared with uninfected animals, infected mice had a significant increase in the inflammatory response during the first 4 days, peaking 2-3 days post-challenge, 40.3% vs. 0.0% and 41.8% vs. 0.7%, respectively. This inflammatory infiltrate was composed mainly of neutrophils and macrophages with a few eosinophils and lymphocytes. An increase in the intensity of immunofluorescence (IF) for ICAM-1 was also observed during days 1-4. ICAM-1 was present in bronchiolar epithelium, type II pneumocytes, and macrophages, as well as on vascular endothelium. The control animals presented ICAM-1 constitutively. In infected mice, VCAM-1 was only observed on vascular endothelium during the first 2 days, with some macrophages expressing this molecule throughout the study periods. CD18 and Mac-1 but not LFA-1 were expressed with a high intensity on neutrophils and macrophages present in the inflammatory infiltrate. In addition, we observed a significant decrease in Colony forming units (CFUs) after the first 2 days post-challenge. These findings suggest that during these early stages, up-regulation of ICAM-1, VCAM-1, CD18 and Mac-1 expression occurs, participating in the inflammatory process and as such, in the pathogenesis of paracoccidioidomycosis (PCM).
authors.affiliation: Medical and Experimental Mycology Group, Corporación para Investigaciones Biológicas (CIB); Carrera 72 A No 78 B 141, A.A. 73 78, Medellín, Colombia, South America. agonzalezm@cib.org.co
authors.forename: Angel
authors.initials: A
authors.lastname: Gonzalez
authors.forename: Henrique L
authors.initials: HL
authors.lastname: Lenzi
authors.forename: Ester M
authors.initials: EM
authors.lastname: Motta
authors.forename: Luzia
authors.initials: L
authors.lastname: Caputo
authors.forename: Jorge H
authors.initials: JH
authors.lastname: Sahaza
authors.forename: Ana M
authors.initials: AM
authors.lastname: Cock
authors.forename: Ana C
authors.initials: AC
authors.lastname: Ruiz
authors.forename: Angela
authors.initials: A
authors.lastname: Restrepo
authors.forename: Luz E
authors.initials: LE
authors.lastname: Cano
mesh_terms: D000818:Animals; D018821:CD18 Antigens / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D008168:Lung / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology; D016169:Lymphocyte Function-Associated Antigen-1 / Q000378:metabolism; D016177:Macrophage-1 Antigen / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010228:Paracoccidioides / Q000472:pathogenicity*; D010229:Paracoccidioidomycosis / Q000276:immunology* / Q000382:microbiology / Q000503:physiopathology*; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D018821:CD18 Antigens; D015815:Cell Adhesion Molecules; D016169:Lymphocyte Function-Associated Antigen-1; D016177:Macrophage-1 Antigen; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1