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Toll-Like Receptor Signaling Reveals Differential Gene Expression Profiles Involved in Prevention of Virus-Induced Asthma
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A5493 - Toll-Like Receptor Signaling Reveals Differential Gene Expression Profiles Involved in Prevention of Virus-Induced Asthma
Author Block: S. Wali1, J. R. Flores Gonzalez2, M. J. Tuvim2, B. F. Dickey2, S. E. Evans2; 1Pulmonary Medicine, MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences, Houston, TX, United States, 2Pulmonary Medicine, University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Introduction: Respiratory viruses are frequent mediators of asthma development and exacerbations. However, there are gaps in understanding how viral infections cause immuno-pathology in the host leading to asthma progression. We have shown that treatment with Toll-like Receptor (TLR) 2/6 and 9 agonists (Pam2-ODN) inhibits viral replication and progression of asthma by reduction in IL-33, airway hyperreactivity and mucus metaplasia. The aim of this study was to identify the molecular host factors that were altered with the treatment and viral infection in mouse model of asthma. Methods: Mice were treated with Pam2-ODN one day prior to Sendai virus infection. Mouse lung RNA collected from day 49 of infection was subjected to RNA sequencing for analysis of host factors and compared between sham-treated, Pam2-ODN treated, Pam2-ODN treated and infected, untreated and infected mice. Results: We have characterized the asthmatic transcriptome of the mouse lungs in the chronic phase of infection and found up-regulation of genes involved in airway remodelling, epithelial cell differentiation and chemokine signalling. More importantly, we identified genes from the treatment group that are involved in reversing the infection effect on day 49. Conclusions: Pam2-ODN treatment led to reduced asthmatic phenotype in Sendai virus-induced mouse model. We have identified several host genes associated with the treatment that are potentially anti-asthmatic in nature. In addition, identification of host genes in the chronic phase of infection provide a better understanding of how viral infections lead to asthmatic progression.
Author Block: S. Wali1, J. R. Flores Gonzalez2, M. J. Tuvim2, B. F. Dickey2, S. E. Evans2; 1Pulmonary Medicine, MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences, Houston, TX, United States, 2Pulmonary Medicine, University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Introduction: Respiratory viruses are frequent mediators of asthma development and exacerbations. However, there are gaps in understanding how viral infections cause immuno-pathology in the host leading to asthma progression. We have shown that treatment with Toll-like Receptor (TLR) 2/6 and 9 agonists (Pam2-ODN) inhibits viral replication and progression of asthma by reduction in IL-33, airway hyperreactivity and mucus metaplasia. The aim of this study was to identify the molecular host factors that were altered with the treatment and viral infection in mouse model of asthma. Methods: Mice were treated with Pam2-ODN one day prior to Sendai virus infection. Mouse lung RNA collected from day 49 of infection was subjected to RNA sequencing for analysis of host factors and compared between sham-treated, Pam2-ODN treated, Pam2-ODN treated and infected, untreated and infected mice. Results: We have characterized the asthmatic transcriptome of the mouse lungs in the chronic phase of infection and found up-regulation of genes involved in airway remodelling, epithelial cell differentiation and chemokine signalling. More importantly, we identified genes from the treatment group that are involved in reversing the infection effect on day 49. Conclusions: Pam2-ODN treatment led to reduced asthmatic phenotype in Sendai virus-induced mouse model. We have identified several host genes associated with the treatment that are potentially anti-asthmatic in nature. In addition, identification of host genes in the chronic phase of infection provide a better understanding of how viral infections lead to asthmatic progression.
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