Characterization of rat lung ICAM-1.
Inflamm Res
; 47(7): 308-15, 1998 Jul.
Article
en En
| MEDLINE
| ID: mdl-9719495
OBJECTIVE AND DESIGN: We expressed soluble rat ICAM-1, generated a polyclonal anti-ICAM-1 antibody, and studied ICAM-1 upregulation in lung inflammatory conditions. Bacterial and baculovirus expression systems were employed. MATERIAL: 250 g adult, male Long Evans rats were used. For in vitro studies, rat pulmonary artery endothelial cells (RPAEC), rat alveolar macrophages and aortic rings were stimulated (as described below) and evaluated for ICAM-1 expression. TREATMENT: RPAEC and macrophages were stimulated with lipopolysaccharide (LPS) and recombinant murine tumour necrosis factor alpha (TNFalpha). In vivo immunoglobulin G (IgG) immune complex-induced lung injury was employed. METHODS: Enzyme-linked immunoassay (ELISA) Western and Northern blot analyses and immunohistochemical evaluations were performed. All experiments were done at least in duplicate. Data were analyzed by two-tailed Student's t-test. RESULTS: ICAM-1 expression of RPAEC was time- and dose-dependent, peaking at 6h after LPS-stimulation. LPS and TNFalpha each enhanced ICAM-1 expression on alveolar macrophages (reaching a maximum at 2 h). In IgG immune complex-induced lung injury, ICAM-1 mRNA isolated from whole lung peaked at 4 h, while lung ICAM- I protein peaked at 6 h. CONCLUSIONS: Quantitation of ICAM-1 expression in vitro and in vivo suggests that ICAM-1 plays a central role in two lung inflammatory models. Furthermore, lung ICAM-1 upregulation involves at least two cell types: vascular endothelial cells and alveolar macrophages.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Molécula 1 de Adhesión Intercelular
/
Pulmón
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Inflamm Res
Asunto de la revista:
ALERGIA E IMUNOLOGIA
/
PATOLOGIA
Año:
1998
Tipo del documento:
Article
País de afiliación:
Estados Unidos
Pais de publicación:
Suiza