Oxidative stress and innate immunity responses in cigarette smoke stimulated nasal epithelial cells

Stefania Gerbino, Serena Di Vincenzo, Elisabetta Pace, Luigi Lanata, Andreina Bruno, Stefania Gerbino, Maria Ferraro, Serena Di Vincenzo, Mark Gjomarkaj

Risultato della ricerca: Article

24 Citazioni (Scopus)

Abstract

Cigarette smoke extracts (CSE) may play a significant role in diseases of the upper airway including chronic rhinosinusitis. Even short term exposure of cigarette smoke has adverse effects on mitochondrial functions and redox homeostasis in tissues which may progress to further complications associated with chronic smoking. Cigarette smoke alters toll-like receptor 4 (TLR4) expression and activation in bronchial epithelial cells. Carbocysteine is an anti-oxidant and mucolytic agent. The effects of carbocysteine on CSE induced oxidative stress and on associated innate immune and inflammatory responses in nasal epithelial cells are largely unknown. The present study was aimed to assess in CSE stimulated nasal epithelial cells (RPMI 2650) the effects of carbocysteine (10(-4)M) on: cell survival, intracellular reactive oxygen species (ROS) production, TLR4 expression, LPS binding and neutrophil chemotaxis (actin reorganization). We found that CSE increased ROS production, TLR4 expression, LPS binding and neutrophil chemotaxis and all these events were counteracted by pre-incubating CSE stimulated RPMI 2650 cells with carbocysteine. In conclusion, the present study provides compelling evidence that carbocysteine may be considered a promising therapeutic strategy in chronic inflammatory nasal diseases.
Lingua originaleEnglish
pagine (da-a)292-299
Numero di pagine8
RivistaToxicology in Vitro
Volume28
Stato di pubblicazionePublished - 2014

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Oxidative stress
Carbocysteine
Nose
Innate Immunity
Smoke
Tobacco Products
Oxidative Stress
Epithelial Cells
Toll-Like Receptor 4
Chemotaxis
Reactive Oxygen Species
Neutrophils
Nose Diseases
Expectorants
Oxidants
Oxidation-Reduction
Actins
Cell Survival
Homeostasis
Smoking

All Science Journal Classification (ASJC) codes

  • Toxicology

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Oxidative stress and innate immunity responses in cigarette smoke stimulated nasal epithelial cells. / Gerbino, Stefania; Di Vincenzo, Serena; Pace, Elisabetta; Lanata, Luigi; Bruno, Andreina; Gerbino, Stefania; Ferraro, Maria; Di Vincenzo, Serena; Gjomarkaj, Mark.

In: Toxicology in Vitro, Vol. 28, 2014, pag. 292-299.

Risultato della ricerca: Article

Gerbino, S, Di Vincenzo, S, Pace, E, Lanata, L, Bruno, A, Gerbino, S, Ferraro, M, Di Vincenzo, S & Gjomarkaj, M 2014, 'Oxidative stress and innate immunity responses in cigarette smoke stimulated nasal epithelial cells', Toxicology in Vitro, vol. 28, pagg. 292-299.
Gerbino, Stefania ; Di Vincenzo, Serena ; Pace, Elisabetta ; Lanata, Luigi ; Bruno, Andreina ; Gerbino, Stefania ; Ferraro, Maria ; Di Vincenzo, Serena ; Gjomarkaj, Mark. / Oxidative stress and innate immunity responses in cigarette smoke stimulated nasal epithelial cells. In: Toxicology in Vitro. 2014 ; Vol. 28. pagg. 292-299.
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abstract = "Cigarette smoke extracts (CSE) may play a significant role in diseases of the upper airway including chronic rhinosinusitis. Even short term exposure of cigarette smoke has adverse effects on mitochondrial functions and redox homeostasis in tissues which may progress to further complications associated with chronic smoking. Cigarette smoke alters toll-like receptor 4 (TLR4) expression and activation in bronchial epithelial cells. Carbocysteine is an anti-oxidant and mucolytic agent. The effects of carbocysteine on CSE induced oxidative stress and on associated innate immune and inflammatory responses in nasal epithelial cells are largely unknown. The present study was aimed to assess in CSE stimulated nasal epithelial cells (RPMI 2650) the effects of carbocysteine (10(-4)M) on: cell survival, intracellular reactive oxygen species (ROS) production, TLR4 expression, LPS binding and neutrophil chemotaxis (actin reorganization). We found that CSE increased ROS production, TLR4 expression, LPS binding and neutrophil chemotaxis and all these events were counteracted by pre-incubating CSE stimulated RPMI 2650 cells with carbocysteine. In conclusion, the present study provides compelling evidence that carbocysteine may be considered a promising therapeutic strategy in chronic inflammatory nasal diseases.",
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T1 - Oxidative stress and innate immunity responses in cigarette smoke stimulated nasal epithelial cells

AU - Gerbino, Stefania

AU - Di Vincenzo, Serena

AU - Pace, Elisabetta

AU - Lanata, Luigi

AU - Bruno, Andreina

AU - Gerbino, Stefania

AU - Ferraro, Maria

AU - Di Vincenzo, Serena

AU - Gjomarkaj, Mark

PY - 2014

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N2 - Cigarette smoke extracts (CSE) may play a significant role in diseases of the upper airway including chronic rhinosinusitis. Even short term exposure of cigarette smoke has adverse effects on mitochondrial functions and redox homeostasis in tissues which may progress to further complications associated with chronic smoking. Cigarette smoke alters toll-like receptor 4 (TLR4) expression and activation in bronchial epithelial cells. Carbocysteine is an anti-oxidant and mucolytic agent. The effects of carbocysteine on CSE induced oxidative stress and on associated innate immune and inflammatory responses in nasal epithelial cells are largely unknown. The present study was aimed to assess in CSE stimulated nasal epithelial cells (RPMI 2650) the effects of carbocysteine (10(-4)M) on: cell survival, intracellular reactive oxygen species (ROS) production, TLR4 expression, LPS binding and neutrophil chemotaxis (actin reorganization). We found that CSE increased ROS production, TLR4 expression, LPS binding and neutrophil chemotaxis and all these events were counteracted by pre-incubating CSE stimulated RPMI 2650 cells with carbocysteine. In conclusion, the present study provides compelling evidence that carbocysteine may be considered a promising therapeutic strategy in chronic inflammatory nasal diseases.

AB - Cigarette smoke extracts (CSE) may play a significant role in diseases of the upper airway including chronic rhinosinusitis. Even short term exposure of cigarette smoke has adverse effects on mitochondrial functions and redox homeostasis in tissues which may progress to further complications associated with chronic smoking. Cigarette smoke alters toll-like receptor 4 (TLR4) expression and activation in bronchial epithelial cells. Carbocysteine is an anti-oxidant and mucolytic agent. The effects of carbocysteine on CSE induced oxidative stress and on associated innate immune and inflammatory responses in nasal epithelial cells are largely unknown. The present study was aimed to assess in CSE stimulated nasal epithelial cells (RPMI 2650) the effects of carbocysteine (10(-4)M) on: cell survival, intracellular reactive oxygen species (ROS) production, TLR4 expression, LPS binding and neutrophil chemotaxis (actin reorganization). We found that CSE increased ROS production, TLR4 expression, LPS binding and neutrophil chemotaxis and all these events were counteracted by pre-incubating CSE stimulated RPMI 2650 cells with carbocysteine. In conclusion, the present study provides compelling evidence that carbocysteine may be considered a promising therapeutic strategy in chronic inflammatory nasal diseases.

KW - CARB, CSE, Cigarette smoke, LPS, Nasal epithelial cells, ROS, Reactive oxygen species, TLR4, carbocysteine, cigarette smoke extracts, lipolysaccharide, reactive oxygen species, toll like receptor 4

UR - http://hdl.handle.net/10447/86387

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JO - Toxicology in Vitro

JF - Toxicology in Vitro

SN - 0887-2333

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