<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Chu HW</submitter><funding>NIAID NIH HHS</funding><funding>NHLBI NIH HHS</funding><pagination>155</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2992501</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Respiratory infections including Mycoplasma pneumoniae (Mp) contribute to various chronic lung diseases. We have shown that mouse short palate, lung, and nasal epithelium clone 1 (SPLUNC1) protein was able to inhibit Mp growth. Further, airway epithelial cells increased SPLUNC1 expression upon Mp infection. However, the mechanisms underlying SPLUNC1 regulation remain unknown. In the current study, we investigated if SPLUNC1 production following Mp infection is regulated through Toll-like receptor 2 (TLR2) signaling.&lt;h4>Methods&lt;/h4>Airway epithelial cell cultures were utilized to reveal the contribution of TLR2 signaling including NF-κB to SPLUNC1 production upon bacterial infection and TLR2 agonist stimulation.&lt;h4>Results&lt;/h4>Mp and TLR2 agonist Pam3CSK4 increased SPLUNC</pubmed_abstract><journal>Respiratory research</journal><pubmed_title>SPLUNC1 regulation in airway epithelial cells: role of Toll-like receptor 2 signaling.</pubmed_title><pmcid>PMC2992501</pmcid><funding_grant_id>P01 HL073907</funding_grant_id><funding_grant_id>R01 AI070175</funding_grant_id><funding_grant_id>R01 HL088264</funding_grant_id><pubmed_authors>Gally F</pubmed_authors><pubmed_authors>Zhang G</pubmed_authors><pubmed_authors>Case S</pubmed_authors><pubmed_authors>Wu Q</pubmed_authors><pubmed_authors>Martin RJ</pubmed_authors><pubmed_authors>Michels N</pubmed_authors><pubmed_authors>Minor M</pubmed_authors><pubmed_authors>Smith S</pubmed_authors><pubmed_authors>Reisdorph N</pubmed_authors><pubmed_authors>Jiang D</pubmed_authors><pubmed_authors>Simon G</pubmed_authors><pubmed_authors>Chu HW</pubmed_authors><pubmed_authors>Janssen-Heininger YM</pubmed_authors><pubmed_authors>Thaikoottathil J</pubmed_authors></additional><is_claimable>false</is_claimable><name>SPLUNC1 regulation in airway epithelial cells: role of Toll-like receptor 2 signaling.</name><description>&lt;h4>Background&lt;/h4>Respiratory infections including Mycoplasma pneumoniae (Mp) contribute to various chronic lung diseases. We have shown that mouse short palate, lung, and nasal epithelium clone 1 (SPLUNC1) protein was able to inhibit Mp growth. Further, airway epithelial cells increased SPLUNC1 expression upon Mp infection. However, the mechanisms underlying SPLUNC1 regulation remain unknown. In the current study, we investigated if SPLUNC1 production following Mp infection is regulated through Toll-like receptor 2 (TLR2) signaling.&lt;h4>Methods&lt;/h4>Airway epithelial cell cultures were utilized to reveal the contribution of TLR2 signaling including NF-κB to SPLUNC1 production upon bacterial infection and TLR2 agonist stimulation.&lt;h4>Results&lt;/h4>Mp and TLR2 agonist Pam3CSK4 increased SPLUNC</description><dates><release>2010-01-01T00:00:00Z</release><publication>2010 Nov</publication><modification>2025-04-04T13:48:25.073Z</modification><creation>2019-03-27T00:36:56Z</creation></dates><accession>S-EPMC2992501</accession><cross_references><pubmed>21054862</pubmed><doi>10.1186/1465-9921-11-155</doi></cross_references></HashMap>