Comprisons of lung tissue gene expression from AKR and C57BL/6 mice exposed to Cigarette smoke and LPS in ARDS/ALI mice model

Our previous study showed that AKR and C57BL/6 mice to cigarette smoke increased lipopolysaccharide (LPS)- induced increased lung vascular permeability. Viremic AKR mice were more susceptible to LPS-induced ALI than C57 on prolonged exposure. In this study we compared the global gene expression patterns to determine the genetic basis for the strain dependent responses to cigarette smoke and LPS-induced ALI. We found AKR transcriptomic responses didnot overlap with C57 mice and AKR mice showed increased responses compared to C57 mice. Global gene expression analysis using microarray was used to dermine the mechanisms of strain dependent responses to cigarette smoking and LPS mediated ALI Two strains of mice (AKR and C57) were exposed to 3 weeks cigarette smoke or room air exposure. Other AKR and C57 mice were exposed to 6 weeks of cigarette smoke or room air exposure, followed by intra-tracheal instillation of LPS in normal saline or NS alone. The lungs were dissected and homgenized and gene expression responses to cigarette smoke and LPS were determined using microarray.