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Cigarette smoke increases BLT 2 receptor functions in bronchial epithelial cells: in vitro and ex vivo evidence
Author(s) -
Pace Elisabetta,
Ferraro Maria,
Vincenzo Serena Di,
Bruno Andreina,
Giarratano Antonino,
Scafidi Valeria,
Lipari Luana,
Benedetto Denise Valentina Di,
Sciarrino Serafina,
Gjomarkaj Mark
Publication year - 2013
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.12077
Subject(s) - neutrophilia , respiratory epithelium , immunology , receptor , bronchoalveolar lavage , stat protein , ex vivo , lung , medicine , chemistry , in vivo , microbiology and biotechnology , biology , signal transduction , stat3
Summary Leukotriene B 4 ( LTB 4 ) is a neutrophil chemotactic molecule with important involvement in the inflammatory responses of chronic obstructive pulmonary disease ( COPD ). Airway epithelium is emerging as a regulator of innate immune responses to a variety of insults including cigarette smoke, the major risk factor for COPD . In this study we have explored whether cigarette smoke extracts ( CSE ) or soluble mediators present in distal lung fluid samples (mini‐bronchoalveolar lavages) from smokers alter the expression of the LTB 4 receptor 2 ( BLT 2) and peroxisome proliferator‐activated receptor‐α ( PPAR ‐α) in bronchial epithelial cells. We also evaluated the effects of CSE on the expression of intercellular adhesion molecule 1 ( ICAM ‐1) and on the binding of signal transducer and activator of transcription 1 ( STAT ‐1) to ICAM ‐1 promoter as well as the adhesiveness of neutrophils to bronchial epithelial cells. CSE and mini‐bronchoalveolar lavages from smokers increased BLT 2 and ICAM ‐1 expression as well as the adhesiveness of neutrophils to bronchial epithelial cells and decreased PPAR ‐α expression. CSE induced the activation of STAT ‐1 and its binding to ICAM ‐1 promoter. These findings suggest that, in bronchial epithelial cells, CSE promote a prevalent induction of pro‐inflammatory BLT 2 receptors and activate mechanisms leading to increased neutrophil adhesion, a mechanism that contributes to airway neutrophilia and to tissue damage.