<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Gong H</submitter><funding>National Natural Science Foundation of China</funding><pagination>6506953</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5603328</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>2017</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>IRAK-M, negatively regulating Toll-like receptor, is shown the dual properties in the varied disease contexts. We studied the effect of IRAK-M deficiency on cigarette smoking- (CS-) induced airway inflammation under acute or subacute conditions in a mouse model.&lt;h4>Methods&lt;/h4>A number of cellular and molecular techniques were used to detect the differences between IRAK-M knockout (KO) and wild type (WT) mice exposed to 3-day or 7-week CS.&lt;h4>Results&lt;/h4>Airway inflammation was comparable between IRAK-M KO and WT mice under 3-day CS exposure. Upon short-term CS exposure and lipopolysaccharide (LPS) inhalation, IRAK-M KO mice demonstrated worse airway inflammation, significantly higher percentage of Th17 cells and concentrations of proinflammatory cytokines in the lungs, </pubmed_abstract><journal>Mediators of inflammation</journal><pubmed_title>Effect of IRAK-M on Airway Inflammation Induced by Cigarette Smoking.</pubmed_title><pmcid>PMC5603328</pmcid><funding_grant_id>81170040</funding_grant_id><funding_grant_id>81470229</funding_grant_id><pubmed_authors>Chen W</pubmed_authors><pubmed_authors>Gao J</pubmed_authors><pubmed_authors>Zhou W</pubmed_authors><pubmed_authors>Liu T</pubmed_authors><pubmed_authors>Gong H</pubmed_authors></additional><is_claimable>false</is_claimable><name>Effect of IRAK-M on Airway Inflammation Induced by Cigarette Smoking.</name><description>&lt;h4>Background&lt;/h4>IRAK-M, negatively regulating Toll-like receptor, is shown the dual properties in the varied disease contexts. We studied the effect of IRAK-M deficiency on cigarette smoking- (CS-) induced airway inflammation under acute or subacute conditions in a mouse model.&lt;h4>Methods&lt;/h4>A number of cellular and molecular techniques were used to detect the differences between IRAK-M knockout (KO) and wild type (WT) mice exposed to 3-day or 7-week CS.&lt;h4>Results&lt;/h4>Airway inflammation was comparable between IRAK-M KO and WT mice under 3-day CS exposure. Upon short-term CS exposure and lipopolysaccharide (LPS) inhalation, IRAK-M KO mice demonstrated worse airway inflammation, significantly higher percentage of Th17 cells and concentrations of proinflammatory cytokines in the lungs, </description><dates><release>2017-01-01T00:00:00Z</release><publication>2017</publication><modification>2025-04-04T09:43:49.511Z</modification><creation>2020-11-19T11:16:54Z</creation></dates><accession>S-EPMC5603328</accession><cross_references><pubmed>28951634</pubmed><doi>10.1155/2017/6506953</doi></cross_references></HashMap>