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

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

Risultato della ricerca: Article

11 Citazioni (Scopus)

Abstract

Leukotriene B4 (LTB4) 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 LTB4 receptor 2 (BLT2) and peroxisome proliferator- activated receptor-a (PPAR-a) 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 minibronchoalveolar lavages from smokers increased BLT2 and ICAM-1 expression as well as the adhesiveness of neutrophils to bronchial epithelial cells and decreased PPAR-a 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 BLT2 receptors and activate mechanisms leading to increased neutrophil adhesion, a mechanism that contributes to airway neutrophilia and to tissue damage.
Lingua originaleEnglish
pagine (da-a)245-255
Numero di pagine11
RivistaImmunology
Volume139
Stato di pubblicazionePublished - 2013

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Smoke
Tobacco Products
Epithelial Cells
Neutrophils
Peroxisome Proliferator-Activated Receptors
Chronic Disease
Leukotriene B4 Receptors
Adhesiveness
Leukotriene B4
Bronchoalveolar Lavage
Transducers
Innate Immunity
Epithelium
In Vitro Techniques
Lung

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

Cita questo

Cigarette smoke increases BLT2 receptor functions in bronchial epithelial cells: in vitro and ex vivo evidence. / Giarratano, Antonino; Scafidi, Valeria; Lipari, Luana; Di Benedetto, Denise Valentina; Bruno, Andreina; Di Vincenzo, Serena; Sciarrino, Serafina; Pace, Elisabetta; Bruno, Andreina; Scafidi, Valeria; Ferraro, Maria; Vincenzo, Serena Di; Gjomarkaj, Mark.

In: Immunology, Vol. 139, 2013, pag. 245-255.

Risultato della ricerca: Article

Giarratano, Antonino ; Scafidi, Valeria ; Lipari, Luana ; Di Benedetto, Denise Valentina ; Bruno, Andreina ; Di Vincenzo, Serena ; Sciarrino, Serafina ; Pace, Elisabetta ; Bruno, Andreina ; Scafidi, Valeria ; Ferraro, Maria ; Vincenzo, Serena Di ; Gjomarkaj, Mark. / Cigarette smoke increases BLT2 receptor functions in bronchial epithelial cells: in vitro and ex vivo evidence. In: Immunology. 2013 ; Vol. 139. pagg. 245-255.
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abstract = "Leukotriene B4 (LTB4) 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 LTB4 receptor 2 (BLT2) and peroxisome proliferator- activated receptor-a (PPAR-a) 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 minibronchoalveolar lavages from smokers increased BLT2 and ICAM-1 expression as well as the adhesiveness of neutrophils to bronchial epithelial cells and decreased PPAR-a 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 BLT2 receptors and activate mechanisms leading to increased neutrophil adhesion, a mechanism that contributes to airway neutrophilia and to tissue damage.",
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AU - Giarratano, Antonino

AU - Scafidi, Valeria

AU - Lipari, Luana

AU - Di Benedetto, Denise Valentina

AU - Bruno, Andreina

AU - Di Vincenzo, Serena

AU - Sciarrino, Serafina

AU - Pace, Elisabetta

AU - Bruno, Andreina

AU - Scafidi, Valeria

AU - Ferraro, Maria

AU - Vincenzo, Serena Di

AU - Gjomarkaj, Mark

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N2 - Leukotriene B4 (LTB4) 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 LTB4 receptor 2 (BLT2) and peroxisome proliferator- activated receptor-a (PPAR-a) 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 minibronchoalveolar lavages from smokers increased BLT2 and ICAM-1 expression as well as the adhesiveness of neutrophils to bronchial epithelial cells and decreased PPAR-a 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 BLT2 receptors and activate mechanisms leading to increased neutrophil adhesion, a mechanism that contributes to airway neutrophilia and to tissue damage.

AB - Leukotriene B4 (LTB4) 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 LTB4 receptor 2 (BLT2) and peroxisome proliferator- activated receptor-a (PPAR-a) 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 minibronchoalveolar lavages from smokers increased BLT2 and ICAM-1 expression as well as the adhesiveness of neutrophils to bronchial epithelial cells and decreased PPAR-a 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 BLT2 receptors and activate mechanisms leading to increased neutrophil adhesion, a mechanism that contributes to airway neutrophilia and to tissue damage.

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