Cigarette smoke increases BLT2 receptor functions in bronchial epithelial cells: in vitro and ex vivo evidence

Serena Di Vincenzo, Antonino Giarratano, Valeria Scafidi, Valeria Scafidi, Maria Ferraro, Serena Di Vincenzo, Mark Gjomarkaj, Serafina Sciarrino, Elisabetta Pace, Andreina Bruno, Andreina Bruno, Denise Valentina Di Benedetto, Luana Lipari

Risultato della ricerca: Articlepeer review

14 Citazioni (Scopus)


Leukotriene B4 (LTB4) is a neutrophil chemotactic molecule with importantinvolvement in the inflammatory responses of chronic obstructivepulmonary disease (COPD). Airway epithelium is emerging as a regulatorof innate immune responses to a variety of insults including cigarettesmoke, the major risk factor for COPD. In this study we have exploredwhether cigarette smoke extracts (CSE) or soluble mediators present indistal lung fluid samples (mini-bronchoalveolar lavages) from smokersalter the expression of the LTB4 receptor 2 (BLT2) and peroxisome proliferator-activated receptor-a (PPAR-a) in bronchial epithelial cells. We alsoevaluated the effects of CSE on the expression of intercellular adhesionmolecule 1 (ICAM-1) and on the binding of signal transducer and activatorof transcription 1 (STAT-1) to ICAM-1 promoter as well as theadhesiveness of neutrophils to bronchial epithelial cells. CSE and minibronchoalveolarlavages from smokers increased BLT2 and ICAM-1expression as well as the adhesiveness of neutrophils to bronchial epithelialcells and decreased PPAR-a expression. CSE induced the activation ofSTAT-1 and its binding to ICAM-1 promoter. These findings suggest that,in bronchial epithelial cells, CSE promote a prevalent induction ofpro-inflammatory BLT2 receptors and activate mechanisms leading toincreased neutrophil adhesion, a mechanism that contributes to airwayneutrophilia and to tissue damage.
Lingua originaleEnglish
pagine (da-a)245-255
Numero di pagine11
Stato di pubblicazionePublished - 2013

All Science Journal Classification (ASJC) codes

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  • ???subjectarea.asjc.2400.2403???


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