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Titolo:
Attenuation of lung inflammation and fibrosis in interferon-gamma-deficient mice after intratracheal bleomycin
Autore:
Chen, ES; Greenlee, BM; Wills-Karp, M; Moller, DR;
Indirizzi:
Johns Hopkins Univ, Dept Med, Div Pulm & Crit Care Med, Baltimore, MD 21224 USA Johns Hopkins Univ Baltimore MD USA 21224 re Med, Baltimore, MD 21224 USA Johns Hopkins Univ, Dept Environm Hlth Sci, Baltimore, MD 21224 USA Johns Hopkins Univ Baltimore MD USA 21224 th Sci, Baltimore, MD 21224 USA
Titolo Testata:
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
fascicolo: 5, volume: 24, anno: 2001,
pagine: 545 - 555
SICI:
1044-1549(200105)24:5<545:AOLIAF>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
INDUCED PULMONARY FIBROSIS; MESSENGER-RNA EXPRESSION; IFN-GAMMA; HYPERSENSITIVITY PNEUMONITIS; GRANULOMA-FORMATION; NITRIC-OXIDE; IN-VIVO; T-CELLS; MOUSE; COLLAGEN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Moller, DR Johns Hopkins Univ, Dept Med, Div Pulm & Crit Care Med, 5501 Hopkins Bayview Circle,JHAAC 4A-60, Baltimore, MD 21224 USA Johns Hopkins Univ 5501 Hopkins Bayview Circle,JHAAC 4A-60 Baltimore MD USA 21224
Citazione:
E.S. Chen et al., "Attenuation of lung inflammation and fibrosis in interferon-gamma-deficient mice after intratracheal bleomycin", AM J RESP C, 24(5), 2001, pp. 545-555

Abstract

Because mouse strains susceptible to bleomycin, such as C57BL/6J, tend to produce T helper type 1 (Th1) cytokines in response to immune activation, we hypothesized that the inflammatory response to bleomycin is mediated, in part, by local production of the Th1 cytokine interferon-gamma (IFN-gamma). Consistent with this hypothesis, fibrosis-prone C57BL/6J and A/J mice demonstrated significantly elevated expression of IFN-gamma protein (by enzyme-linked immunosorbent assay) in bronchoalveolar lavage fluid at 24 h, and subsequently increased lung inflammation, weight loss, and mortality 10 d after intratracheal bleomycin administration compared with fibrosis-resistant BALB/c mice or saline control mice. To directly determine a role for IFN-gamma in bleomycin toxicity, we exposed C57BL/6J mice with a homozygous null mutation of the IFN-gamma gene (IFN-gamma[-/-]) and wildtype C57BL/6J mice to intratracheal bleomycin. IFN-gamma(-/-) mice demonstrated significantly lower parenchymal inflammation, weight loss, and mortality 10 d after 5 U/kg intratracheal bleomycin administration compared with control mice. At 3 wk after 1.5 U/kg bleomycin exposure, single lung collagen determined by hydroxyproline assay was significantly lower in IFN-gamma(-/-) mice compared with wild-type C57BL/6J mice. Together, these results suggest that IFN-gammamediates, in part, bleomycin-induced pulmonary inflammation and fibrosis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 03:49:21