Wood smoke enhances cigarette smoke-induced inflammation by inducing the aryl hydrocarbon receptor repressor in airway epithelial cells.

摘要: Our previous studies showed that cigarette smokers who are exposed to wood smoke (WS) at an increased risk for chronic bronchitis and reduced lung function. The present study was undertaken determine the mechanisms WS-induced adverse effects. We studied effect of WS exposure using four cohorts mice. C57Bl/6 mice were 4 or 12 weeks filtered air, 10 mg/m(3) 2 h/d, 250 (CS) 6 CS followed by (CW). Inflammation absent in air groups, but enhanced twofold bronchoalveolar lavage CW compared with group as measured neutrophil numbers levels chemoattractant, keratinocyte-derived chemokine. anti-inflammatory lipoxin, lipoxin A4, threefold along cyclo-oxygenase (COX)-2 microsomal prostaglandin E synthase (mPGES)-1 airway epithelial cells PGE2 replicated, primary human cells, changes observed Immunoprecipitations blocked interaction aryl hydrocarbon receptor (AHR) AHR nuclear transporter reduce expression COX-2 mPGES-1 increasing repressor (AHRR). Collectively, these show low concentrations CS-induced inflammation inducing AHRR suppress AHR, COX-2, expression, A4. Therefore, is a potential therapeutic target WS-associated exacerbations inflammation.