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Titolo:
Interaction of cigarette smoke and house dust mite allergens on inflammatory mediator release from primary cultures of human bronchial epithelial cells
Autore:
Rusznak, C; Sapsford, RJ; Devalia, JL; Shah, SS; Hewitt, EL; Lamont, AG; Davies, RJ; Lozewicz, S;
Indirizzi:
St Bartholomews & Royal London Sch Med & Dent, Acad Dept Resp Med, London,England St Bartholomews & Royal London Sch Med & Dent London England on,England London Chest Hosp, Dept Cardiovasc Surg, London E2 9JX, England London Chest Hosp London England E2 9JX asc Surg, London E2 9JX, England Peptide Therapeut Plc, Cambridge, England Peptide Therapeut Plc Cambridge England erapeut Plc, Cambridge, England
Titolo Testata:
CLINICAL AND EXPERIMENTAL ALLERGY
fascicolo: 2, volume: 31, anno: 2001,
pagine: 226 - 238
SICI:
0954-7894(200102)31:2<226:IOCSAH>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
PASSIVE SMOKING; LUNG-FUNCTION; IN-VITRO; CHILDREN; ASTHMA; EXPOSURE; PERMEABILITY; GLUTATHIONE; RESPONSES;
Keywords:
cigarette smoke; house dust mite allergens; inflammatory mediators;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: Rusznak, C Vanderbilt Univ, Med Ctr, Vanderbilt Allergy Ctr, 2611 W End Ave, Nashville, TN 37203 USA Vanderbilt Univ 2611 W End Ave Nashville TN USA 37203 37203 USA
Citazione:
C. Rusznak et al., "Interaction of cigarette smoke and house dust mite allergens on inflammatory mediator release from primary cultures of human bronchial epithelial cells", CLIN EXP AL, 31(2), 2001, pp. 226-238

Abstract

Background Several studies have shown that exposure to cigarette smoke and/or house dust mite (HDM) can lead to increased airway inflammation in susceptible individuals. The underlying mechanisms, however, are not defined. Objective To investigate the interaction between cigarette smoke and HDM allergen on mediator release from primary cultures of human bronchial epithelial cells. Methods Confluent human bronchial epithelial cell cultures were exposed tocigarette smoke in the absence or presence of HDM allergen and investigated for the release of IL-8, IL-1 beta, and sICAM-1. Damage to the epithelialcells themselves was assessed by release of Cr-51. On separate occasions, we investigated the effect of PTL11028, a highly patent and selective Der p1 inhibitor, on HDM allergen-induced release of IL-8, following activation of HDM allergen by incubation with cysteine. The effect of cigarette smoke exposure on the stability of these released mediators in prepared solutionsin the absence/presence of reduced glutathione was also studied. Results Both HDM allergens and short-term (20 min) cigarette smoke exposure led to a significantly increased release of IL-8, IL-1 beta and sICAM-1 from the epithelial cell cultures. Longer exposure (1-6 h) to cigarette smoke led to a dramatic decrease in the amount of these mediators detected in the culture medium. Whilst incubation of epithelial cultures with HDM allergen did not cause any significant change in the release of Cr-51 from pre-loaded cells, cigarette smoke on its own led to a marked, exposure and incubation-time dependent increase in the release of Cr-51. Incubation with HDM allergen led to a significant, dose and time-dependent increase in the release of IL-8, which was further enhanced when the allergen extract was pre-activated with cysteine. This effect was completely abrogated by PTL11028, a novel Der p1 inhibitor. Prepared solutions of various concentrations of IL-8, IL-1 beta and sICAM-1 exposed to cigarette smoke demonstrated a dramaticexposure time-dependent decrease in the detectable amount of these mediators, an effect which was abrogated by GSH. Conclusions HDM-induced airway inflammation may include DET p-mediated release of inflammatory mediators from epithelial cells. Additionally, short-term cigarette smoke exposure may induce airway inflammation by release of inflammatory mediators from these cells, an effect which may be potentiated by Der p allergens. Longer term cigarette smoke exposure may cause damage to epithelial cells and changes in the structure of inflammatory mediators.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 08/08/20 alle ore 08:43:54