Project description:To investigate the impact of cigarette smoke on lung gene expression, female BALB/c mice were obtained from Charles River at 6-8 weeks of age. Using a whole body exposure system (SIU48, PROMECH LAB AB, Vintrie, Sweden), mice (5 per group) were exposed to room air or the mainstream cigarette smoke of twelve 3R4F reference cigarettes (University of Kentucky, Lexington, USA) with filters removed 5 days per week, twice daily for 50 minutes/exposure for 8 weeks, as previously described. Control animals were exposed to room air only. Lungs were collected and stored in RNALater at -80M-BM-0C prior to RNA extraction. Impact of an 8 week cigarette smoke exposure on BALB/c mouse lung gene expression was assessed.
Project description:To investigate the impact of cigarette smoke on lung gene expression, female BALB/c mice were obtained from Charles River at 6-8 weeks of age. Using a whole body exposure system (SIU48, PROMECH LAB AB, Vintrie, Sweden), mice (5 per group) were exposed to room air or the mainstream cigarette smoke of twelve 3R4F reference cigarettes (University of Kentucky, Lexington, USA) with filters removed 5 days per week, twice daily for 50 minutes/exposure for 8 weeks, as previously described. Control animals were exposed to room air only. Lungs were collected and stored in RNALater at -80°C prior to RNA extraction.
Project description:We have investigated the effects of cigarette smoke exposure in three different strains of mice. DBA/2 and C57Bl/6J are susceptible to smoke and develop different lung changes in response to chronic exposure, while ICR mice are resistant to smoke and do not develop emphysema. The present study was carried out to determine early changes in the gene expression profile of mice exposed to cigarette smoke with either a susceptible or resistant phenotype. Experiment Overall Design: Three strains of mice were exposed to smoke from three cigarette/day, 5d/wk for 4 weeks. Microarray analysis was carried out on total RNA extracted from the lung utilizing the Affymetrix platform.
Project description:To identify biosignatures that describe these lifestyle susceptibility factors, we performed parallel exposures of regular weight (RW) C57BL/6 and diet-induced obese (DIO) C57BL/6 mice to cigarette smoke, either mainstream (MS) or sidestream (SS), mimicking both the smoker and environmental exposure through second-hand smoke, respectively. Transcriptional responses were measured by global microarray analysis of lung tissue. Groups (N=8 biological replicates) of RW and DIO C57BL/6 mice (15-weeks old at start of exposures) were exposed to either filtered air (sham controls, SC), mainstream (MS) or sidestream (SS) cigarette smoke by nose-only inhalation exposure for 5 hr/day for a total of eight exposures over two weeks as follows: 5 consecutive days of exposure, followed by 2 days with no exposure, then three days of exposure, with necropsies occurring the day following the last exposure.
Project description:COPD is a disorder characterized by the progressive development of airflow limitation that is not fully reversible. Cigarette smoke has been generally accepted as the most important of many risk factors for the development of COPD. We used microarray technology to perform comprehensive gene expression profiling of smoke exposure and cessation effects in mouse muscle tissue. Mice received nose-only exposure of 4% mainstream cigarette smoke or air (sham exposure) for 2 hours/day, 5 days/week for 2, 12 or 24 weeks. Mice undergoing smoke cessation received cigarette smoke exposure for 12 weeks, and then sham exposure for 12 weeks.
Project description:These studies tested the hypotheses that smoke induces changes in mRNA profiles that are dependent on sex and the health status of the lung, and that the effects of smoke are different after 1 day compared to 5 days of smoke exposure. The ways in which the lungs modulate their response to cigarette smoke after repeated exposures are important for understanding the toxicology of smoke, for developing biomarkers of chronic smoke exposure, and for understanding the therapeutic potential in regulatory signaling pathways that are beneficial or detrimental to lung health. Sex-matched 5-7-week old wildtype (WT) and Scnn1b-overexpressing (BENaC) littermates were exposed to cigarette smoke or sham (room air) exposure. Exposure occurred in a plexiglass chamber attached to a smoke delivery device using an exposure chamber and smoking machine (inExpose Exposure System, SCIREQ, Chandler, AZ). Mice were exposed to mainstream + sidestream smoke from 6 reference cigarettes with filters removed per day (3R4F research cigarettes, University of Kentucky). Each cigarette was puffed for 2 sec every 25 sec, using the standard Federal Trade Commission smoking machine protocol. The sham-exposed control mice were exposed to room air in the exposure chamber for a time equivalent to that needed for active smoke exposure. Mice were exposed to cigarette or sham smoke for 1 day or 5 consecutive days. Samples were harvested 4 hours after the completion of the final smoke exposure. The right lung was used for gene expression analysis.
Project description:We have investigated the effects of cigarette smoke exposure in three different strains of mice. DBA/2 and C57Bl/6J are susceptible to smoke and develop different lung changes in response to chronic exposure, while ICR mice are resistant to smoke and do not develop emphysema. The present study was carried out to determine early changes in the gene expression profile of mice exposed to cigarette smoke with either a susceptible or resistant phenotype.
Project description:In the context of male reproductive health, epidemiological studies have observed reduced testis size and abnormal sperm counts and morphology in adult men exposed in utero, although these findings are not always repeated. The ambiguity of these reports is confounded by a lack of controlled animal studies investigating the effects of maternal cigarette smoke exposure on male offspring reproductive health. In this study we examined the effects of cigarette induced reproductive toxicity on male offspring exposed during the gestational and weaning period using our novel direct nasal exposure mouse model of cigarette smoke-induced chronic obstructive pulmonary disease and female subfertility. This was done too gain a better understanding of the adverse effects of gestational maternal smoking on male offspring fertility. C57BL/6 5 week-old female mice were exposed via the nose-only to cigarette smoke [twelve 3R4F reference cigarettes (University of Kentucky, USA) twice/day, five times per week, for 12-18 weeks]. Each exposure lasted 60 minutes. Control mice received room air. In total, 27 mice underwent cigarette smoke exposure. Eleven week-old female mice exposed to cigarette smoke for 6 weeks were separated into groups of three and housed with a single control stud male aged 7-8 weeks with proven fertility for a maximum of 12 weeks. Females were monitored every second day for post-coital plugs and pregnancy. Pregnant females were separated into single cages and litter sizes/pup weights recorded. Smoke exposure via dams continued throughout mating/pregnancy/lactation until weaning of pups at 21days post birth. The testis of exposed offspring were then collected for RNA extraction and hybridization on an Illumina Sentrix Mouse ref-8 v2 Beadchip
Project description: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