Profiling fibrotic lung in TGFb1-Tg mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE31950 | GEO | 2013/03/22
SECONDARY ACCESSION(S): PRJNA155289
REPOSITORIES: GEO
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Project description:Rhinovirus infections exacerbate chronic respiratory inflammatory diseases such as asthma and chronic obstructive pulmonary disease (COPD). Airway epithelial cells are the primary site of rhinovirus replication and responsible for initiating the host immune response to infection. Numerous studies have reported that the anti-viral innate immune response in asthma is deficient leading to the conclusion that epithelial innate immunity is a key determinant of disease severity during a rhinovirus induced exacerbation. However, deficient rhinovirus-induced epithelial interferon production in asthma has not always been observed. We hypothesised that disparate in vitro airway epithelial infection models lacking genome-wide, time-course analyses have obscured the role of epithelial innate anti-viral immunity in asthma and COPD. To address this, we developed a low multiplicity of infection (MOI) rhinovirus model of differentiated primary epithelial cells obtained from healthy, asthma and COPD donors. Using genome-wide gene expression following infection, we demonstrated that gene expression patterns are similar across patient groups, but that the kinetics of induction are delayed in cells obtained from asthma and COPD donors. Rhinovirus-induced innate immune responses were defined by interferons (type-I, II and III), interferon response factors (IRF1, IRF3 and IRF7), TLR signalling and NF‐kB and STAT1 activation. Induced gene expression was evident at 24 hours and peaked at 48 hours post‐infection in cells from healthy subjects. In contrast, in cells from donors with asthma or COPD induction was maximal at or beyond 72-96 hours post infection. Thus, we propose that propensity for viral exacerbations of asthma and COPD relate to delayed (rather than deficient) expression of epithelial cell innate anti-viral immune genes which in turns leads to a delayed and ultimately more inflammatory host immune response.
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Project description:This program aims at identifying the lung gene signature associated with inflammation and emphysema in IL-1b-Tg mouse COPD model to facilitate understanding of the disease mechanism and therapeutic compound testing The lung profiling data was analyzed by identifying genes that were up- and down-regulated at selected p value and fold change in the lungs of IL-1b-Tg mice treated with doxycycline (to induce IL-1b transgene) compared to the corresponding water-treated controls.
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Project description:Background: Tissue remodeling induced by airway inflammation is a main trigger of pathogenesis in various chronic lung diseases like asthma, COPD, IPF, and pulmonary hypertension. The role of human airway smooth muscle cells (HASMCs) in this context is unclear. Hypothesis: HASMCs participate in linking inflammation with remodeling. Methods: The inflammatory responses of ex vivo-cultivated HASMCs to TNFα were investigated by whole-genome-microarray analyses. Diferrential regulation of genes associated with airway inflammation and remodeling were verified by qRT-PCR and ELISA. Results: TNFa induced the expression of 18 cytokines/chemokines and five tissue remodeling genes involved in (severe/corticosteroid-insensitive) asthma, COPD, IPF and/or pulmonary hypertension. Conclusion: HASMCs participate in the interaction of inflammation and tissue remodeling. HASMCs might be considered as targets in therapies of chronic inflammatory lung diseases with regard to attenuating inflammation-induced remodeling processes leading to the development of emphysema or fibrosis. HASMCs of eight donors were left untreated of were stimulated with TNFa at 20 ng/ml. Total RNA was subjected after eight hours of stimulation to whole-human-genome oligo microarray analysis.
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