<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Li J</submitter><funding>National Natural Sciences Foundation of China</funding><pagination>103</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10082527</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>24(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Epithelial barrier is important for asthma development by shaping immune responses. Airway expressing-IL-1 receptor-associated kinase (IRAK)-M of Toll-like receptor pathway was involved in immunoregulation of airway inflammation through influencing activities of macrophages and dendritic cells or T cell differentiation. Whether IRAK-M has effect on cellular immunity in airway epithelial cells upon stimulation remains unclear.&lt;h4>Methods&lt;/h4>We modeled cellular inflammation induced by IL-1β, TNF-α, IL-33, and house dust mite (HDM) in BEAS-2B and A549 cells. Cytokine production and pathway activation were used to reflect the effects of IRAK-M siRNA knockdown on epithelial immunity. Genotyping an asthma-susceptible IRAK-M SNP rs1624395 and measurement of serum CXCL10 levels</pubmed_abstract><journal>Respiratory research</journal><pubmed_title>IRAK-M has effects in regulation of lung epithelial inflammation.</pubmed_title><pmcid>PMC10082527</pmcid><funding_grant_id>81170040</funding_grant_id><funding_grant_id>30470767</funding_grant_id><funding_grant_id>81470229</funding_grant_id><funding_grant_id>81970025</funding_grant_id><pubmed_authors>Zheng Z</pubmed_authors><pubmed_authors>Liu Y</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Zhang H</pubmed_authors><pubmed_authors>Gao J</pubmed_authors></additional><is_claimable>false</is_claimable><name>IRAK-M has effects in regulation of lung epithelial inflammation.</name><description>&lt;h4>Background&lt;/h4>Epithelial barrier is important for asthma development by shaping immune responses. Airway expressing-IL-1 receptor-associated kinase (IRAK)-M of Toll-like receptor pathway was involved in immunoregulation of airway inflammation through influencing activities of macrophages and dendritic cells or T cell differentiation. Whether IRAK-M has effect on cellular immunity in airway epithelial cells upon stimulation remains unclear.&lt;h4>Methods&lt;/h4>We modeled cellular inflammation induced by IL-1β, TNF-α, IL-33, and house dust mite (HDM) in BEAS-2B and A549 cells. Cytokine production and pathway activation were used to reflect the effects of IRAK-M siRNA knockdown on epithelial immunity. Genotyping an asthma-susceptible IRAK-M SNP rs1624395 and measurement of serum CXCL10 levels</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Apr</publication><modification>2026-05-29T01:09:50.219Z</modification><creation>2024-11-15T20:01:52.192Z</creation></dates><accession>S-EPMC10082527</accession><cross_references><pubmed>37029363</pubmed><doi>10.1186/s12931-023-02406-5</doi></cross_references></HashMap>