Full transcriptome and proteome analysis of the mechanism of tuberculosis Ag85B-Fc2a in alleviating allergic asthma in mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE269136 | GEO | 2025/06/05
REPOSITORIES: GEO
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Project description:In the early stage, an OVA-induced mouse allergic asthma model was constructed and treated with ESAT6-Fc2a fusion protein, which proved that ESAT6-Fc2a fusion protein could reduce the infiltration of inflammatory cells in the lungs and had a therapeutic effect on asthma. In order to further explore the mechanism of action, we carried out transcriptomics sequencing, screened out related genes, enriched them, and focused on pathways with significant differences. In the later stage, q-PCR experiments will be performed for verification.
2025-06-05 | GSE274427 | GEO
Project description:In the early stage, an OVA-induced mouse allergic asthma model was constructed and treated with Ag85B-Fc2a fusion protein, which proved that Ag85B-Fc2a fusion protein could reduce the infiltration of inflammatory cells in the lungs and had a therapeutic effect on asthma。In order to further explore the mechanism of action, we carried out transcriptomics and proteomic sequencing, screened out related genes and proteins, enriched them, and focused on pathways with significant differences. In the later stage, q-PCR and Western-blot experiments will be performed for verification.
2024-06-04 | PXD052816 |
Project description:Asthma bronchiale is an inflammatory disease of the respiratory airways and a major factor of increasing health care costs worldwide. The molecular actors leading to asthma are not fully understood and require further investigation. The aim of this study was to monitor the proteome during asthma development from early inflammatory to late fibrotic stages. A time-course-based ovalbumin (OVA) mouse model was applied to establish an asthma phenotype and the lung proteome was analysed at four time points during asthma development (0 weeks = control, 5 weeks, 8 weeks and 12 weeks of OVA treatment).
2021-02-11 | PXD011159 | Pride
Project description:Background: Inhalation exposure to biological particulate matter (BioPM) from livestock farms may provoke exacerbations in subjects suffering from allergy and asthma. The aim of this study was to use a murine model of allergic asthma to determine the effect of BioPM derived from goat farm on airway allergic responses Methods: Fine (< 2.5 μm) BioPM was collected from an indoor goat stable. Female BALB/c mice were ovalbumin (OVA) sensitized and challenged with OVA or saline as control. The OVA and saline groups were divided in sub-groups and exposed intranasally to different concentrations (0, 0.9, 3, or 9 μg) of goat farm BioPM. Bronchoalveolar lavage fluid (BALF), blood and lung tissues were collected. Results: In saline-challenged mice, goat farm BioPM alone induced a dose-dependent increase in neutrophils in BALF and induced production of macrophage inflammatory protein-3a). In OVA-challenged mice, BioPM significantly enhanced 1) inflammatory cells in BALF, 2) OVA-specific Immunoglobulin (Ig)G1, 3) interleukin-23 production, 4) airway mucus secretion-specific gene expression. RNAseq analysis of lungs indicates that neutrophil chemotaxis and oxidation-reduction processes were the representative genomic pathways in saline and OVA-challenged mice, respectively. Conclusions: A single exposure to goat farm BioPM enhanced airway inflammation in both saline and OVA-challenged allergic mice, with neutrophilic response as Th17 disorder and eosinophilic response as Th2 disorder indicative of the severity of allergic responses. Identification of the mode of action by which farm PM interacts with airway allergic pathways will be useful to design potential therapeutic approaches.
2020-08-01 | GSE148240 | GEO
Project description:The objective of the study was to present a transcriptome-wide m6A methylome profile of lung tissues in mouse model of ovalbumin(OVA)-induced acute allergic asthma.
2021-10-11 | GSE179874 | GEO
Project description:Humans vary markedly in their propensity to develop asthma, despite often being exposed to similar environmental stimuli. Similarly, mouse strains vary in susceptibility to airways pathology in experimental asthma. Sensitization and aerosol challenge with ovalbumin (OVA) induces eosinophil accumulation, mucus production and airways obstruction in BALB/c and C57BL/6 mice. In contrast, CBA/Ca mice show relatively little pathology. Allergen-induced production of IL-4, IL-5, IL-10 and IFN-g was detected in all three strains, with BALB/c mice generating the highest levels of IL-4, IL-5 and IL-10. Microarray analysis was used to identify genes differentially regulated in lung tissue after OVA challenge. Differentially regulated genes in the lungs of the asthma-susceptible C57BL/6 and BALB/c strains numbered 242 and 145, respectively, whereas only 42 genes were differentially expressed in the resistant CBA/Ca strain. In C57BL/6 mice, transcripts were enriched for adhesion molecules and this was associated with high levels of eosinophil recruitment. Differentially regulated genes in the lungs of only the asthma-susceptible strains numbered 64 and several of these have not previously been associated with asthma. Many of the genes differentially regulated in the susceptible strains were enzymes involved in inflammation. Using network analysis, mRNA for the anti-apoptotic protein survivin was found to be up-regulated in the lungs following allergen challenge. Survivin mRNA and protein were also expressed at high levels in eosinophils recovered by bronchoalveolar lavage from BALB/c and C57BL/6 mice. We propose that rapid apoptosis of lung eosinophils due to low expression of survivin contributes to the limitation of pathology in CBA/Ca mice Humans vary markedly in their propensity to develop asthma, despite often being exposed to similar environmental stimuli. Similarly, mouse strains vary in susceptibility to airways pathology in experimental asthma. Sensitization and aerosol challenge with ovalbumin (OVA) induces eosinophil accumulation, mucus production and airways obstruction in BALB/c and C57BL/6 mice. In contrast, CBA/Ca mice show relatively little pathology. Allergen-induced production of IL-4, IL-5, IL-10 and IFN-g was detected in all three strains, with BALB/c mice generating the highest levels of IL-4, IL-5 and IL-10. Microarray analysis was used to identify genes differentially regulated in lung tissue after OVA challenge. Differentially regulated genes in the lungs of the asthma-susceptible C57BL/6 and BALB/c strains numbered 242 and 145, respectively, whereas only 42 genes were differentially expressed in the resistant CBA/Ca strain. In C57BL/6 mice, transcripts were enriched for adhesion molecules and this was associated with high levels of eosinophil recruitment. Differentially regulated genes in the lungs of only the asthma-susceptible strains numbered 64 and several of these have not previously been associated with asthma. Many of the genes differentially regulated in the susceptible strains were enzymes involved in inflammation. Using network analysis, mRNA for the anti-apoptotic protein survivin was found to be up-regulated in the lungs following allergen challenge. Survivin mRNA and protein were also expressed at high levels in eosinophils recovered by bronchoalveolar lavage from BALB/c and C57BL/6 mice. We propose that rapid apoptosis of lung eosinophils due to low expression of survivin contributes to the limitation of pathology in CBA/Ca mice Changes in gene expression in the lungs of 4 individual of BALB/c mice challenged with OVA were monitored using the lungs of 4 individual BALB/c mice challenged with PBS as the control. The microarray analysis was performed in quadruplicate. Changes in gene expression in the lungs of 4 individual of CBA/Ca mice challenged with OVA were monitored using the lungs of 4 individual CBA/Ca mice challenged with PBS as the control. The microarray analysis was performed in quadruplicate. Changes in gene expression in the lungs of 4 individual of BALB/c mice challenged with OVA were monitored using the lungs of 4 individual CBA/Ca mice challenged with OVA as the control. The microarray analysis was performed in quadruplicate. Twelve dual channel microarray slides were used in the overall design of this experiment.
2010-05-18 | E-GEOD-15345 | biostudies-arrayexpress
Project description:Humans vary markedly in their propensity to develop asthma, despite often being exposed to similar environmental stimuli. Similarly, mouse strains vary in susceptibility to airways pathology in experimental asthma. Sensitization and aerosol challenge with ovalbumin (OVA) induces eosinophil accumulation, mucus production and airways obstruction in BALB/c and C57BL/6 mice. In contrast, CBA/Ca mice show relatively little pathology. Allergen-induced production of IL-4, IL-5, IL-10 and IFN-g was detected in all three strains, with BALB/c mice generating the highest levels of IL-4, IL-5 and IL-10. Microarray analysis was used to identify genes differentially regulated in lung tissue after OVA challenge. Differentially regulated genes in the lungs of the asthma-susceptible C57BL/6 and BALB/c strains numbered 242 and 145, respectively, whereas only 42 genes were differentially expressed in the resistant CBA/Ca strain. In C57BL/6 mice, transcripts were enriched for adhesion molecules and this was associated with high levels of eosinophil recruitment. Differentially regulated genes in the lungs of only the asthma-susceptible strains numbered 64 and several of these have not previously been associated with asthma. Many of the genes differentially regulated in the susceptible strains were enzymes involved in inflammation. Using network analysis, mRNA for the anti-apoptotic protein survivin was found to be up-regulated in the lungs following allergen challenge. Survivin mRNA and protein were also expressed at high levels in eosinophils recovered by bronchoalveolar lavage from BALB/c and C57BL/6 mice. We propose that rapid apoptosis of lung eosinophils due to low expression of survivin contributes to the limitation of pathology in CBA/Ca mice Humans vary markedly in their propensity to develop asthma, despite often being exposed to similar environmental stimuli. Similarly, mouse strains vary in susceptibility to airways pathology in experimental asthma. Sensitization and aerosol challenge with ovalbumin (OVA) induces eosinophil accumulation, mucus production and airways obstruction in BALB/c and C57BL/6 mice. In contrast, CBA/Ca mice show relatively little pathology. Allergen-induced production of IL-4, IL-5, IL-10 and IFN-g was detected in all three strains, with BALB/c mice generating the highest levels of IL-4, IL-5 and IL-10. Microarray analysis was used to identify genes differentially regulated in lung tissue after OVA challenge. Differentially regulated genes in the lungs of the asthma-susceptible C57BL/6 and BALB/c strains numbered 242 and 145, respectively, whereas only 42 genes were differentially expressed in the resistant CBA/Ca strain. In C57BL/6 mice, transcripts were enriched for adhesion molecules and this was associated with high levels of eosinophil recruitment. Differentially regulated genes in the lungs of only the asthma-susceptible strains numbered 64 and several of these have not previously been associated with asthma. Many of the genes differentially regulated in the susceptible strains were enzymes involved in inflammation. Using network analysis, mRNA for the anti-apoptotic protein survivin was found to be up-regulated in the lungs following allergen challenge. Survivin mRNA and protein were also expressed at high levels in eosinophils recovered by bronchoalveolar lavage from BALB/c and C57BL/6 mice. We propose that rapid apoptosis of lung eosinophils due to low expression of survivin contributes to the limitation of pathology in CBA/Ca mice Changes in gene expression in the lungs of 4 individual of BALB/c mice challenged with OVA were monitored using the lungs of 4 individual BALB/c mice challenged with PBS as the control. The microarray analysis was performed in quadruplicate. Changes in gene expression in the lungs of 4 individual of CBA/Ca mice challenged with OVA were monitored using the lungs of 4 individual CBA/Ca mice challenged with PBS as the control. The microarray analysis was performed in quadruplicate. Changes in gene expression in the lungs of 4 individual of BALB/c mice challenged with OVA were monitored using the lungs of 4 individual CBA/Ca mice challenged with OVA as the control. The microarray analysis was performed in quadruplicate. Twelve dual channel microarray slides were used in the overall design of this experiment.
2010-05-18 | E-GEOD-15414 | biostudies-arrayexpress
Project description:RATIONALE: In a mouse model of maternal transmission of asthma risk (J. Immunol 170:1683, 2003), baby mice of asthmatic (As), but not normal (Nrm), mothers show increased susceptibility to allergy. We previously showed that adoptive transfer to normal baby mice of dendritic cells (DCs) harvested from asthma-susceptible but allergen-naïve neonates reproduces the increased susceptibility to asthma. Hence, the maternal effect is mediated by altered neonatal DCs, which skew immune responses towards a pro-allergic Th2 phenotype. To identify potential molecular mechanisms, we performed epigenomic profiling of isolated neonatal DCs. METHODS: BALB/c mice were sensitized by 2 i.p. injections of ovalbumin (OVA) in alum and repeatedly challenged with OVA aerosols (As) prior to mating with normal males. Purified splenic CD11c+ DCs of 14-day old allergen-naïve offspring from these As and control Nrm mothers were isolated using magnetic beads. Methylation profiles of genomic DNA were obtained using Switchgear epigenomic chip arrays. After normalization and background correction analysis using significance analysis for microarrays (SAM) and ANOVA was performed. RESULTS: We identified 300 to 6000 (depending on stringency) chromosomal regions with significantly different methylation status, (2 â 10 fold). Clustering methods and pathway analysis identified several interrelated gene groups that merit further study. CONCLUSION: Maternal asthma causes multiple significant epigenetic changes in neonatal dendritic cells. Keywords: Dendritic cells, genomic DNA, DNA methylation, allergy, asthma The analysis includes 9 samples of genomic DNA from isolated splenic CD11c+ dendritic cells (>95% pure) per group. The two groups are neonates born to mothers with induced allergy to ovalbumin, and normal control neonates. All neonates are genetically and environmentally identical, and allergen-naive.
2010-06-24 | E-GEOD-13380 | biostudies-arrayexpress
Project description:Diesel exhaust (DE) has been shown to enhance allergic sensitization in animals following high dose instillation or chronic inhalation exposure scenarios. The purpose of this study was to determine if short term exposures to diluted DE enhance allergic immune responses to antigen, and identify possible mechanisms using microarray technology. BALB/c mice were exposed to filtered air or diluted DE to yield particle concentrations of 500 or 2000 µg/m3 4 hr/day on days 0-4. Mice were sensitized intranasally with ovalbumin (OVA) antigen or saline on days 0-2, and 18 and all were challenged with OVA on day 28. Mice were necropsied either 4 hrs after the last DE exposure on day 4, or 18, 48, and 96 hrs after challenge. Immunological endpoints included OVA-specific serum IgE, biochemical and cellular profiles of bronchoalveolar lavage (BAL), and cytokine production in the BAL. OVA-sensitized mice exposed to both concentrations of DE had increased eosinophils, neutrophils, lymphocytes, and IL-6 post-challenge compared to OVA control, while DE/saline exposure yielded increases in neutrophils at the high dose only. Microarray analysis demonstrated distinct gene expression profiles for the high dose DE/OVA and DE/saline groups. DE/OVA induced pathways involved in oxidative stress and metabolism while DE in the absence of allergen sensitization modulated cell cycle control, growth and differentiation, G-proteins, and cell adhesion pathways. This study shows for the first time early changes in gene expression induced by the combination of diesel exhaust inhalation and antigen sensitization, which resulted in stronger development of an allergic asthma phenotype. Experiment Overall Design: Lung RNA was isolated from mice exposed to filtered air, 500 ug/m3 DE, or 2000 ug/m3 DE with or without OVA for a total of 6 exposure groups. Each group had 4 replicates for a total of 24 microarrays.
2008-06-16 | E-GEOD-9383 | biostudies-arrayexpress
Project description:RATIONALE: In a mouse model of maternal transmission of asthma risk (J. Immunol 170:1683, 2003), baby mice of asthmatic (As), but not normal (Nrm), mothers show increased susceptibility to allergy. We previously showed that adoptive transfer to normal baby mice of dendritic cells (DCs) harvested from asthma-susceptible but allergen-naïve neonates reproduces the increased susceptibility to asthma. Hence, the maternal effect is mediated by altered neonatal DCs, which skew immune responses towards a pro-allergic Th2 phenotype. To identify potential molecular mechanisms, we performed epigenomic profiling of isolated neonatal DCs. METHODS: BALB/c mice were sensitized by 2 i.p. injections of ovalbumin (OVA) in alum and repeatedly challenged with OVA aerosols (As) prior to mating with normal males. Purified splenic CD11c+ DCs of 14-day old allergen-naïve offspring from these As and control Nrm mothers were isolated using magnetic beads. Methylation profiles of genomic DNA were obtained using Switchgear epigenomic chip arrays. After normalization and background correction analysis using significance analysis for microarrays (SAM) and ANOVA was performed. RESULTS: We identified 300 to 6000 (depending on stringency) chromosomal regions with significantly different methylation status, (2 – 10 fold). Clustering methods and pathway analysis identified several interrelated gene groups that merit further study. CONCLUSION: Maternal asthma causes multiple significant epigenetic changes in neonatal dendritic cells. Keywords: Dendritic cells, genomic DNA, DNA methylation, allergy, asthma
2008-11-04 | GSE13380 | GEO