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Titolo:
Activation of NF-kappa B by PM10 occurs via an iron-mediated mechanism in the absence of I kappa B degradation
Autore:
Jimenez, LA; Thompson, J; Brown, DA; Rahman, I; Antonicelli, F; Duffin, R; Drost, EM; Hay, RT; Donaldson, K; MacNee, W;
Indirizzi:
Univ Edinburgh, Sch Med, Edinburgh Lung & Environm Grp Initiat Colt Res La, Dept Med & Radiol Sci, Edinburgh, Midlothian, Scotland Univ Edinburgh Edinburgh Midlothian Scotland burgh, Midlothian, Scotland Univ St Andrews, Sch Biomed Sci, Edinburgh, Midlothian, Scotland Univ St Andrews Edinburgh Midlothian Scotland urgh, Midlothian, Scotland Napier Univ, Dept Life Sci, Edinburgh EH14 1DJ, Midlothian, Scotland Napier Univ Edinburgh Midlothian Scotland EH14 1DJ , Midlothian, Scotland
Titolo Testata:
TOXICOLOGY AND APPLIED PHARMACOLOGY
fascicolo: 2, volume: 166, anno: 2000,
pagine: 101 - 110
SICI:
0041-008X(20000715)166:2<101:AONBBP>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
PARTICULATE AIR-POLLUTION; TUMOR-NECROSIS-FACTOR; OBSTRUCTIVE PULMONARY-DISEASE; ULTRAFINE CARBON-BLACK; LUNG EPITHELIAL-CELLS; FREE-RADICAL ACTIVITY; ALVEOLAR MACROPHAGES; TRANSCRIPTION FACTOR; ENZYMATIC OXIDATION; GENE-EXPRESSION;
Keywords:
PM10; NF-kappa B; I kappa B; iron; A549 cells; endotoxin;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: MacNee, W Univ Edinburgh, Sch Med, Edinburgh Lung & Environm Grp Initiat Colt Res La, Dept Med & Radiol Sci, Teviot Pl, Edinburgh, Midlothian, Scotland Univ Edinburgh Teviot Pl Edinburgh Midlothian Scotland Scotland
Citazione:
L.A. Jimenez et al., "Activation of NF-kappa B by PM10 occurs via an iron-mediated mechanism in the absence of I kappa B degradation", TOX APPL PH, 166(2), 2000, pp. 101-110

Abstract

Exposure to particulate air pollution (PM10) is associated with exacerbations of respiratory diseases and increased cardiopulmonary mortality. PM10 induces lung inflammation in rats, which has been attributed to many factors, including the ultrafine components of PM10, endotoxins, and transition metals. In this study, we investigated in alveolar epithelial (A549) cells whether PM10 could activate nuclear factor-kappa B (NF-kappa B), a transcription factor stimulated in response to many proinflammatory agents. Our results show that PM10 samples from various sites within the United Kingdom cause nuclear translocation, DNA-binding, and transcriptional activation of NF-kappa B in A549 cells. Furthermore, increased NF-kappa B activity was observed in the absence of I kappa B degradation. To evaluate the role of iron, A549 cells were exposed to PM10 previously treated with phosphate-buffered saline (PBS), deferoxamine mesylate, or deferoxamine plus ferrozine. PBS-treated and, to a lesser extent, deferoxamine-treated PM10 were able to activate NF-kappa B, whereas this response was completely abrogated in cells exposed to PM10 treated with both deferoxamine and ferrozine. Moreover, we studied the effects of soluble components of PM10 on NF-kappa B activation by exposing alveolar epithelial cells to soluble fractions from PM10 treated with PBS or the metal chelators. We found that, compared with fractions fromPBS-treated PM10 which activated NF-kappa B, fractions from PM10 treated with deferoxamine and ferrozine did not stimulate NF-kappa B activity above background levels. Coincubation of polymixin B, an endotoxin-binding compound, and PR10 did not inhibit NF-kappa B. In summary, PM10 activates NF-kappa B in A549 cells by an iron-mediated mechanism in the absence of I kappa Bdegradation. (C) 2000 Academic Press.

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Documento generato il 01/12/20 alle ore 11:03:48