Expression data from mouse lungs, exposed in-utero to second-hand smoke (SHS) and challenged with ovalbumin (OVA) as adults.
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE38409 | GEO | 2012/06/02
SECONDARY ACCESSION(S): PRJNA167827
REPOSITORIES: GEO
Similar Datasets
Project description:SHS exposure during pregnancy has adverse effects on offspring. We used microarrays to characterize the gene expression changes caused by in-utero SHS exposure and adult (19-23 weeks) OVA challenge in 23-week mouse lungs. Left lungs from Balb/c male and female mice were collected at 23 weeks of age for RNA extraction and hybridization on Affymetrix mouse 430 2.0 microarrays. Based on the gender differences and in-utero exposure status, there are 4 groups of mice, females and males, exposed in-utero to filtered-air or SHS. All were exposure to OVA (19-23 weeks). We extracted RNA from 4 animals from each group for microarray analysis (total N = 16 samples).
2012-06-01 | E-GEOD-38409 | biostudies-arrayexpress
Project description:Second-hand smoke (SHS) exposure during pregnancy has adverse effects on offspring. We used microarrays to characterize the gene expression changes caused by in-utero exposure and adult exposure to SHS in adult mouse lungs.
2012-03-27 | GSE36810 | GEO
Project description:Second-hand smoke (SHS) exposure during pregnancy has adverse effects on offspring. We used microarrays to characterize the gene expression changes caused by in-utero exposure and adult exposure to SHS in adult mouse lungs. Left lungs from Balb/c male mice were collected at 15 weeks of age for RNA extraction and hybridization on Affymetrix mouse 430 2.0 microarrays. Based on their smoke exposure status, there are 4 groups of mice, each exposed in-utero to filtered-air or SHS and as an adult to filtered-air or SHS. We extracted RNA from 4 animals from each group for microarray analysis (N = 16 samples).
2012-03-26 | E-GEOD-36810 | biostudies-arrayexpress
Project description:Second-hand smoke (SHS) exposure in utero exacerbates adult responses to environmental irritants. We tested the hypothesis that effects of in utero SHS exposure on modulating physiological and transcriptome responses in BALB/c mouse lungs after ovalbumin (OVA) challenge extend well into adulthood, and that the responses show a sex bias. We exposed BALB/c mice in utero to SHS or filtered air (AIR), then sensitized and challenged all offspring with OVA from 19 to 23 weeks of age. At the end of the adult OVA challenge, we evaluated pulmonary function, examined histopathology, analyzed bronchoalveolar lavage fluid (BALF), and assessed gene expression changes in the lung samples. All groups exhibited lung inflammation and inflammatory cell infiltration. Pulmonary function testing (airway hyperresponsiveness [AHR], breathing frequency [f]) and BALF (cell differentials, Th1/Th2 cytokines) assessments showed significantly more pronounced lung responses in the SHS-OVA groups than in AIR-OVA groups (AHR, f; eosinophils, neutrophils; IFN-γ, IL-1b, IL-4, IL-5, IL-10, IL-13, KC/CXCL1, TNF-α), with the majority of responses being more pronounced in males than in females. SHS exposure in utero also significantly altered lung gene expression profiles, primarily of genes associated with inflammatory responses and respiratory diseases, including lung cancer and lung fibrosis. Altered expression profiles of chemokines (Cxcl2, Cxcl5, Ccl8, Ccl24), cytokines (Il1b, Il6, Il13) and acute phase response genes (Saa1, Saa3) were confirmed by qRT-PCR. In conclusion, in utero exposure to SHS exacerbates adult lung responses to OVA challenge and promotes a pro-asthmatic milieu in adult lungs; further, males are generally more affected by SHS-OVA than are females.
| S-EPMC3931120 | biostudies-literature
Project description:In utero exposure to second-hand smoke (SHS) is associated with exacerbated asthmatic responses in children. We tested the hypothesis that in utero SHS will aggravate the lung responses of young adult mice re-exposed to SHS. We exposed Balb/c mice in utero to SHS (S) or filtered air (AIR; A), and re-exposed the male offspring daily from 11-15 weeks of age to either SHS (AS and SS) or AIR (AA and SA). After the adult exposures, we analyzed samples of bronchoalveolar lavage fluid (BALF), examined the results of histopathology, and assessed pulmonary function and gene expression changes in lung samples. In SS mice, compared with the other three groups (AA, AS, and SA), we found decreases in breathing frequency and increases in airway hyperresponsiveness (AHR), as well as low but significantly elevated concentrations of BALF proinflammatory cytokines (IL-1b, IL-6, and keratinocyte-derived chemokine). Lung morphometric analyses revealed enlarged airspaces and arteries in SA and SS mice compared with their in utero AIR counterparts, as well as increased collagen deposition in AS and SS mice. Unique gene expression profiles were found for in utero, adult, and combined exposures, as well as for mice with elevated AHR responses. The profibrotic metalloprotease genes, Adamts9 and Mmp3, were up-regulated in the SS and AHR groups, suggesting a role for in utero SHS exposure on the adult development of chronic obstructive pulmonary disease. Our results indicate that in utero exposures to environmentally relevant concentrations of SHS alter lung structure more severely than do adult SHS exposures of longer duration. These in utero exposures also aggravate AHR and promote a profibrotic milieu in adult lungs.
| S-EPMC3547098 | biostudies-literature
Project description:In this study, we have investigated the role of secondhand smoke (SHS) in the development of metabolic liver disease by characterizing the global regulation of genes and molecular pathways in SHS-exposed mice after termination of exposure (SHS 4M) and following one-month recovery in clean air (SHS 4M +1M RECOVERY).
2020-03-23 | GSE139440 | GEO
Project description:A large body of evidence has linked secondhand smoke (SHS) to lung cancer in nonsmokers. Yet, the underlying mechanisms of SHS carcinogenicity in nonsmokers' lung cancer remain elusive. Recently, we have demonstrated a genotoxic mode of action for SHS, based on the ability of this carcinogen to induce adduct-driven mutagenesis in transgenic Big Blue® mice. In the present study, we have expanded this investigation to determine whether SHS can also cause epigenetic effects through aberrations of DNA methylation. Here, we have globally profiled DNA methylation in the lung of Big Blue® mice exposed to SHS for a duration of 4-months, both immediately after the termination of exposure and at several intervals post-exposure.
2012-11-29 | GSE41421 | GEO
Project description:A large body of evidence has linked secondhand smoke (SHS) to lung cancer in nonsmokers. Yet, the underlying mechanisms of SHS carcinogenicity in nonsmokers' lung cancer remain elusive. Recently, we have demonstrated a genotoxic mode of action for SHS, based on the ability of this carcinogen to induce adduct-driven mutagenesis in transgenic Big Blue® mice. In the present study, we have expanded this investigation to determine whether SHS can also cause epigenetic effects through aberrations of DNA methylation. Here, we have globally profiled DNA methylation in the lung of Big Blue® mice exposed to SHS for a duration of 4-months, both immediately after the termination of exposure and at several intervals post-exposure. We have used a genome-wide microarray-based approach to catalogue DNA methylation profile in the lung of mice exposed to SHS and at various recovery periods from the time of exposure. Mice exposed to clean air, for comparable amount of times, were used as controls. Mice that were injected intraperitoneally with chronic doses of B(a)P (a powerful carcinogen in SHS) or DMSO (sham) were used for comparison purposes .
2012-11-29 | E-GEOD-41421 | biostudies-arrayexpress
Project description:This program aims at identifying the lung gene signature associated with OVA-challenged mouse asthma model to facilitate understanding of the disease mechanism and therapeutic compound testing
2013-03-22 | GSE31949 | GEO
Project description:To gain insight into the promoting effect of ultrafine particle inhalation on development and progression of allergic asthma, we selected an experimental approach involving exposure to ultrafine carbon particles (UCP) and gene expression profiling of lungs from mice with experimental, ovalbumin induced allergy. Comparative gene expression analysis was performed by hybridizing pooled cDNA samples from lavaged lungs of different groups. The results suggest that allergic sensitization may represent an susceptibility factor for effects of UCP on gene expression in the lung. In sensitized individuals UCP exposure, such as found in polluted air, thus may contribute to the development and/or aggrevation of allergic asthma. Keywords: Particle Inhalation, lung, ovalbumin sensitized and challanged, expression profling
2007-07-01 | GSE6571 | GEO