Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Inhibition of neutrophil apoptosis by acrolein: a mechanism of tobacco-related lung disease?
Autore:
Finkelstein, EI; Nardini, M; Van der Vliet, A;
Indirizzi:
Univ Calif Davis, Sch Med, Dept Internal Med, Ctr Comparat Resp Biol & Med, Davis, CA 95616 USA Univ Calif Davis Davis CA USA 95616 Resp Biol & Med, Davis, CA 95616 USA Natl Inst Food & Nutr Res, Rome, Italy Natl Inst Food & Nutr Res Rome Italy Inst Food & Nutr Res, Rome, Italy
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
fascicolo: 3, volume: 281, anno: 2001,
pagine: L732 - L739
SICI:
1040-0605(200109)281:3<L732:IONABA>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGRAMMED CELL-DEATH; CIGARETTE-SMOKE; NADPH OXIDASE; POLYMORPHONUCLEAR LEUKOCYTES; GLUTATHIONE DEPLETION; ALVEOLAR MACROPHAGES; OXIDATIVE STRESS; INFLAMMATION; INVOLVEMENT; RESOLUTION;
Keywords:
aldehyde; inflammation; interleukin-8; caspase-3;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Van der Vliet, A Univ Calif Davis, Sch Med, Dept Internal Med, Ctr Comparat Resp Biol & Med, 1121 Surge 1, Davis, CA 95616 USA Univ Calif Davis 1121 Surge 1 Davis CA USA 95616 5616 USA
Citazione:
E.I. Finkelstein et al., "Inhibition of neutrophil apoptosis by acrolein: a mechanism of tobacco-related lung disease?", AM J P-LUNG, 281(3), 2001, pp. L732-L739

Abstract

Cigarette smoking is known to contribute to inflammatory diseases of the respiratory tract by promoting recruitment of inflammatory-immune cells suchas neutrophils and perhaps by altering neutrophil functional properties. We investigated whether acrolein, a toxic unsaturated aldehyde found in cigarette smoke, could directly affect neutrophil function. Exposure of freshlyisolated human neutrophils to acrolein markedly inhibited spontaneous neutrophil apoptosis as indicated by loss of membrane asymmetry and DNA fragmentation and induced increased neutrophil production of the chemokine interleukin-8 (IL-8). Acrolein (1-50 muM) was found to induce marked activation ofextracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinases (MAPKs), and inhibition of p38 MAPK activation by SB-203580 prevented acrolein-induced IL-8 release. However, inhibition of either ERK or p38 MAPK did not affect acrolein-dependent inhibition of apoptosis. Acrolein exposure prevented the activation of caspase-3, a crucial step in the execution of neutrophil apoptosis, presumably by direct inhibition of the enzyme. Our results indicate that acrolein may contribute to smoke-induced inflammatory processes in the lung by increasing neutrophil recruitment and reducing neutrophil clearance by apoptosis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/07/20 alle ore 20:43:25