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Titolo:
Involvement of phosphoinositide 3-kinases in neutrophil activation and thedevelopment of acute lung injury
Autore:
Yum, HK; Arcaroli, J; Kupfner, J; Shenkar, R; Penninger, JM; Sasaki, T; Yang, KY; Park, JS; Abraham, E;
Indirizzi:
Univ Colorado, Hlth Sci Ctr, Div Pulm Sci & Crit Care Med, Denver, CO 80262 USA Univ Colorado Denver CO USA 80262 i & Crit Care Med, Denver, CO 80262 USA Univ Toronto, Dept Med Biophys, Toronto, ON, Canada Univ Toronto Toronto ON Canada to, Dept Med Biophys, Toronto, ON, Canada Univ Toronto, Dept Immunol, Toronto, ON, Canada Univ Toronto Toronto ON Canada oronto, Dept Immunol, Toronto, ON, Canada Univ Toronto, Ontario Canc Inst, Amgen Inst, Toronto, ON, Canada Univ Toronto Toronto ON Canada anc Inst, Amgen Inst, Toronto, ON, Canada
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 11, volume: 167, anno: 2001,
pagine: 6601 - 6608
SICI:
0022-1767(200112)167:11<6601:IOP3IN>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
NF-KAPPA-B; RESPIRATORY-DISTRESS SYNDROME; INDUCED PULMONARY-EDEMA; TUMOR-NECROSIS-FACTOR; IN-VIVO; PHOSPHATIDYLINOSITOL 3-KINASE; SIGNAL-TRANSDUCTION; KINASE-B; ALVEOLAR MACROPHAGES; MONONUCLEAR-CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: Abraham, E Univ Colorado, Hlth Sci Ctr, Div Pulm Sci & Crit Care Med, 4200E 9th Ave,Box C272, Denver, CO 80262 USA Univ Colorado 4200 E 9th Ave,Box C272 Denver CO USA 80262 2 USA
Citazione:
H.K. Yum et al., "Involvement of phosphoinositide 3-kinases in neutrophil activation and thedevelopment of acute lung injury", J IMMUNOL, 167(11), 2001, pp. 6601-6608

Abstract

Activated neutrophils contribute to the development and severity of acute lung injury (ALI). Phosphoinositide 3-kinases (PI3-K) and the downstream serine/threonine kinase Akt/protein kinase B have a central role in modulating neutrophil function, including respiratory burst, chemotaxis, and apoptosis. In the present study, we found that exposure of neutrophils to endotoxin resulted in phosphorylation. of Akt, activation of NF-kappaB and expression of the proinflammatory cytokines IL-1 beta and TNF-a through PI3-K-dependent pathways. In vivo, endotoxin administration to mice resulted in activation of PI3-K and Akt in neutrophils that accumulated in the lungs. The severity of endotoxemia-induced ALI was significantly diminished in mice lacking the p110 gamma catalytic subunit of PI3-K. In PI3-K gamma (-/-) mice, lung edema, neutrophil recruitment, nuclear translocation of NF-kappaB and pulmonary levels of IL-1 beta and TNF-alpha were significantly lower after endotoxemia as compared with PI3-K gamma (+/+) controls. Among neutrophils that did accumulate in the lungs of the PI3-K gamma (-/-) mice after endotoxin administration, activation of NF-kappaB and expression of proinflammatorycytokines was diminished compared with levels present in lung neutrophils from PI3-K gamma (+/+) mice. These results show that PI3-K, and particularly PI3-K gamma, occupies a central position in regulating endotoxin-induced neutrophil activation, including that involved in ALI.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/07/20 alle ore 21:55:32