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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, OBJECTIVE, METHODS, RESULTS. Meshes: Bronchi, Cells, Cultured, Chemokine CXCL10, Epithelial Cells, Humans, Immunity, Innate, Interferon-beta, Interleukin-8, Rhinovirus, Smoke, Tobacco.
user
Does brief exposure to cigarette smoke impair airway epithelial cell innate anti-viral defence? Context: 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. To determine the impact of short-term exposure to cigarette smoke on innate immune responses of airway epithelial cells infected with hRV. 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. CSE induced a concentration-dependent decrease in CXCL10 (p<0.001) and IFN-β (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-β treatment at t=0 after infection blunts the effects of CSE on viral replication (p<0.05).
assistant
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. Final Decision: yes