{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kang YJ"],"funding":["NIAID NIH HHS","NHLBI NIH HHS"],"pagination":["e1000934"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2880565"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["6(6)"],"pubmed_abstract":["Intestinal epithelial cells (IECs) compose the first barrier against microorganisms in the gastrointestinal tract. Although the NF-kappaB pathway in IECs was recently shown to be essential for epithelial integrity and intestinal immune homeostasis, the roles of other inflammatory signaling pathways in immune responses in IECs are still largely unknown. Here we show that p38alpha in IECs is critical for chemokine expression, subsequent immune cell recruitment into the intestinal mucosa, and clearance of the infected pathogen. Mice with p38alpha deletion in IECs suffer from a sustained bacterial burden after inoculation with Citrobacter rodentium. These animals are normal in epithelial integrity and immune cell function, but fail to recruit CD4(+) T cells into colonic mucosal lesions. The ex"],"journal":["PLoS pathogens"],"pubmed_title":["Epithelial p38alpha controls immune cell recruitment in the colonic mucosa."],"pmcid":["PMC2880565"],"funding_grant_id":["AI68896","T32 HL007195-32","T32 HL007195","R01 AI041637","R01 AI068896","AI41637"],"pubmed_authors":["Hong L","van den Berg A","Zhang DW","Kang YJ","Otsuka M","Huang Z","Han J","Vallance BA","Tobias PS","Wu X"],"additional_accession":[]},"is_claimable":false,"name":"Epithelial p38alpha controls immune cell recruitment in the colonic mucosa.","description":"Intestinal epithelial cells (IECs) compose the first barrier against microorganisms in the gastrointestinal tract. Although the NF-kappaB pathway in IECs was recently shown to be essential for epithelial integrity and intestinal immune homeostasis, the roles of other inflammatory signaling pathways in immune responses in IECs are still largely unknown. Here we show that p38alpha in IECs is critical for chemokine expression, subsequent immune cell recruitment into the intestinal mucosa, and clearance of the infected pathogen. Mice with p38alpha deletion in IECs suffer from a sustained bacterial burden after inoculation with Citrobacter rodentium. These animals are normal in epithelial integrity and immune cell function, but fail to recruit CD4(+) T cells into colonic mucosal lesions. The ex","dates":{"release":"2010-01-01T00:00:00Z","publication":"2010 Jun","modification":"2026-05-03T03:23:52.499Z","creation":"2026-05-03T03:13:29.705Z"},"accession":"S-EPMC2880565","cross_references":{"pubmed":["20532209"],"doi":["10.1371/journal.ppat.1000934"]}}