<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Hazan G</submitter><funding>NHLBI NIH HHS</funding><funding>Children&amp;apos;s Discovery Institute</funding><funding>HHS | NIH | National Heart, Lung, and Blood Institute</funding><pagination>1467-1482</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8917060</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>208(6)</volume><pubmed_abstract>Asthma is a chronic disease of childhood, but for unknown reasons, disease activity sometimes subsides as children mature. In this study, we present clinical and animal model evidence suggesting that the age dependency of childhood asthma stems from an evolving host response to respiratory viral infection. Using clinical data, we show that societal suppression of respiratory virus transmission during coronavirus disease 2019 lockdown disrupted the traditional age gradient in pediatric asthma exacerbations, connecting the phenomenon of asthma remission to virus exposure. In mice, we show that asthmatic lung pathology triggered by Sendai virus (SeV) or influenza A virus is highly age-sensitive: robust in juvenile mice (4-6 wk old) but attenuated in mature mice (>3 mo old). Interestingly, all</pubmed_abstract><journal>Journal of immunology (Baltimore, Md. : 1950)</journal><pubmed_title>Age-Dependent Reduction in Asthmatic Pathology through Reprogramming of Postviral Inflammatory Responses.</pubmed_title><pmcid>PMC8917060</pmcid><funding_grant_id>R01 HL135846</funding_grant_id><funding_grant_id>R35 HL145242</funding_grant_id><funding_grant_id>R01 HL152245</funding_grant_id><funding_grant_id>R01 HL152968</funding_grant_id><funding_grant_id>PD-II-2016-529</funding_grant_id><pubmed_authors>Wu K</pubmed_authors><pubmed_authors>White M</pubmed_authors><pubmed_authors>Kau AL</pubmed_authors><pubmed_authors>Eiden E</pubmed_authors><pubmed_authors>Kelley D</pubmed_authors><pubmed_authors>Keeler SP</pubmed_authors><pubmed_authors>Byers D</pubmed_authors><pubmed_authors>Eubanks A</pubmed_authors><pubmed_authors>Alexander-Brett J</pubmed_authors><pubmed_authors>Atkinson J</pubmed_authors><pubmed_authors>Koenitzer JR</pubmed_authors><pubmed_authors>Haspel J</pubmed_authors><pubmed_authors>Steinberg D</pubmed_authors><pubmed_authors>Hernandez-Leyva A</pubmed_authors><pubmed_authors>Agapov E</pubmed_authors><pubmed_authors>Anderson N</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Fox C</pubmed_authors><pubmed_authors>Holtzman MJ</pubmed_authors><pubmed_authors>Hazan G</pubmed_authors><pubmed_authors>Gierasch C</pubmed_authors><pubmed_authors>Rosen AL</pubmed_authors></additional><is_claimable>false</is_claimable><name>Age-Dependent Reduction in Asthmatic Pathology through Reprogramming of Postviral Inflammatory Responses.</name><description>Asthma is a chronic disease of childhood, but for unknown reasons, disease activity sometimes subsides as children mature. In this study, we present clinical and animal model evidence suggesting that the age dependency of childhood asthma stems from an evolving host response to respiratory viral infection. Using clinical data, we show that societal suppression of respiratory virus transmission during coronavirus disease 2019 lockdown disrupted the traditional age gradient in pediatric asthma exacerbations, connecting the phenomenon of asthma remission to virus exposure. In mice, we show that asthmatic lung pathology triggered by Sendai virus (SeV) or influenza A virus is highly age-sensitive: robust in juvenile mice (4-6 wk old) but attenuated in mature mice (>3 mo old). Interestingly, all</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Mar</publication><modification>2026-05-09T22:14:05.388Z</modification><creation>2024-11-19T16:59:49.272Z</creation></dates><accession>S-EPMC8917060</accession><cross_references><pubmed>35173037</pubmed><doi>10.4049/jimmunol.2101094</doi></cross_references></HashMap>