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Titolo:
Induction of eotaxin expression and release from human airway smooth muscle cells by IL-1 beta and TNF alpha: effects of IL-10 and corticosteroids
Autore:
Chung, KF; Patel, HJ; Fadlon, EJ; Rousell, J; Haddad, EB; Jose, PJ; Mitchell, J; Belvisi, M;
Indirizzi:
Natl Heart & Lung Inst, London SW3 6LY, England Natl Heart & Lung Inst London England SW3 6LY t, London SW3 6LY, England Univ London Imperial Coll Sci Technol & Med, London, England Univ London Imperial Coll Sci Technol & Med London England don, England
Titolo Testata:
BRITISH JOURNAL OF PHARMACOLOGY
fascicolo: 5, volume: 127, anno: 1999,
pagine: 1145 - 1150
SICI:
0007-1188(199907)127:5<1145:IOEEAR>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHEMOKINE EOTAXIN; EOSINOPHILIC INFLAMMATION; GENOMIC ORGANIZATION; EPITHELIAL-CELLS; ATOPIC ASTHMA; MESSENGER-RNA; CC-CHEMOKINE; CYTOKINES; INHIBITION; LUNG;
Keywords:
eotaxin; airway smooth muscle cells; interleukin-10; interleukin-1 beta; interferon-gamma; tumour necrosis factor-alpha;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
28
Recensione:
Indirizzi per estratti:
Indirizzo: Chung, KF Natl Heart & Lung Inst, Dovehouse St, London SW3 6LY, England Natl Heart & Lung Inst Dovehouse St London England SW3 6LY land
Citazione:
K.F. Chung et al., "Induction of eotaxin expression and release from human airway smooth muscle cells by IL-1 beta and TNF alpha: effects of IL-10 and corticosteroids", BR J PHARM, 127(5), 1999, pp. 1145-1150

Abstract

1 Eotaxin is a novel C-C chemokine with selective chemoattractant activityfor eosinophiis. We determined whether eotaxin could be produced by human airway smooth muscle (HASM) cells in culture and examined its regulation byinterleukin-10 (IL-10) and the corticosteroid, dexamethasone.2 Stimulation of the cells with interleukin-1 beta (IL-1 beta) or tumour necrosis factor (TNF alpha) each at 10 ng ml(-1) induced the release of eotaxin protein with maximal accumulation by 24 h. Interferon-gamma (IFN gamma)alone at 10 ng ml(-1) had no effect and there was no synergy between thesecytokines on the release of eotaxin.3 Reverse phase high performance liquid chromatographic (HPLC) analysis ofsupernatents from cells treated with TNF alpha (10 ng ml(-1)) for 96 h showed immunoreactivity to eotaxin which eluted with the expected retention time of 34.5-35 min.4 Both IL-1 beta and TNF alpha-induced release of eotaxin was not inhibited by dexamethasone (1 mu M), however IL-10 (10 ng ml(-1)) had a significantinhibitory effect. Dexamethasone and IL-10 did not inhibit the induction of eotaxin mRNA induced by IL-1 beta or TNF alpha.5 Thus, human airway smooth muscle cells can release eotaxin and could be an important source of chemokine production during airway inflammatory events.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 13:47:45