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Brief exposure to cigarette smoke impairs airway epithelial cell innate anti-viral defence.
Logan, Jayden; Chen, Linping; Gangell, Catherine; Sly, Peter D; Fantino, Emmanuelle; Liu, Kenneth.
Afiliação
  • Logan J; Children's Lung, Environment and Asthma Research Team, Queensland Children's Medical Research Institute, The University of Queensland, Brisbane, Australia.
  • Chen L; Children's Lung, Environment and Asthma Research Team, Queensland Children's Medical Research Institute, The University of Queensland, Brisbane, Australia.
  • Gangell C; Children's Lung, Environment and Asthma Research Team, Queensland Children's Medical Research Institute, The University of Queensland, Brisbane, Australia.
  • Sly PD; Children's Lung, Environment and Asthma Research Team, Queensland Children's Medical Research Institute, The University of Queensland, Brisbane, Australia.
  • Fantino E; Children's Lung, Environment and Asthma Research Team, Queensland Children's Medical Research Institute, The University of Queensland, Brisbane, Australia. Electronic address: e.fantino@uq.edu.au.
  • Liu K; Children's Lung, Environment and Asthma Research Team, Queensland Children's Medical Research Institute, The University of Queensland, Brisbane, Australia.
Toxicol In Vitro ; 28(8): 1430-5, 2014 Dec.
Article em En | MEDLINE | ID: mdl-25111775
ABSTRACT

BACKGROUND:

Human rhinovirus (hRV) infections commonly cause acute upper respiratory infections and asthma exacerbations. Environmental cigarette smoke exposure is associated with a significant increase in the risk for these infections in children.

OBJECTIVE:

To determine the impact of short-term exposure to cigarette smoke on innate immune responses of airway epithelial cells infected with hRV.

METHODS:

A human bronchial epithelial cell line (HBEC-3KT) was exposed to cigarette smoke extract (CSE) for 30 min and subsequently infected with hRV serotype 1B. Viral-induced cytokine release was measured with AlphaLISA and viral replication quantified by shed viral titer and intracellular viral copy number 24h post-infection.

RESULTS:

CSE induced a concentration-dependent decrease in CXCL10 (p<0.001) and IFN-ß (p<0.001), with a 79% reduction at the highest dose with an associated 3-fold increase in shed virus. These effects were maintained when infection was delayed up to 24h post CSE exposure. Exogenous IFN-ß treatment at t=0 after infection blunts the effects of CSE on viral replication (p<0.05).

CONCLUSION:

A single exposure of 30 min to cigarette smoke has a lasting impact on epithelial innate defence providing a plausible mechanism for the increase in respiratory infections seen in children exposed to second-hand tobacco smoke.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Rhinovirus / Fumaça / Nicotiana / Brônquios / Imunidade Inata Limite: Humans Idioma: En Ano de publicação: 2014 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Rhinovirus / Fumaça / Nicotiana / Brônquios / Imunidade Inata Limite: Humans Idioma: En Ano de publicação: 2014 Tipo de documento: Article