<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-06-29T01:19:21Z</responseDate><request verb="GetRecord" identifier="oai:docta.ucm.es:20.500.14352/117343" metadataPrefix="qdc">https://docta.ucm.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:docta.ucm.es:20.500.14352/117343</identifier><datestamp>2025-03-18T15:12:14Z</datestamp><setSpec>com_20.500.14352_14</setSpec><setSpec>col_20.500.14352_15</setSpec></header><metadata><qdc:qualifieddc xmlns:qdc="http://dspace.org/qualifieddc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:doc="http://www.lyncode.com/xoai" xsi:schemaLocation="http://purl.org/dc/elements/1.1/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dc.xsd http://purl.org/dc/terms/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dcterms.xsd http://dspace.org/qualifieddc/ http://www.ukoln.ac.uk/metadata/dcmi/xmlschema/qualifieddc.xsd">
   <dc:title>Macrophage-dependent neutrophil recruitment is impaired under conditions of increased intestinal permeability in JAM-A-deficient mice</dc:title>
   <dc:creator>Luissint, Anny-Claude</dc:creator>
   <dc:creator>Williams, Holly C.</dc:creator>
   <dc:creator>Kim, Wooki</dc:creator>
   <dc:creator>Flemming, Sven</dc:creator>
   <dc:creator>Hilgarth, Roland S.</dc:creator>
   <dc:creator>O'Leary, Monique N.</dc:creator>
   <dc:creator>Denning, Tomothy L.</dc:creator>
   <dc:creator>Nusrat, Asma</dc:creator>
   <dc:creator>Parkos, Charles A.</dc:creator>
   <dc:creator>Azcutia Criado, Verónica</dc:creator>
   <dcterms:abstract>Junctional adhesion molecule-A (JAM-A) is a transmembrane glycoprotein expressed on leukocytes, endothelia, and epithelia that regulates biological processes including barrier function and immune responses. While JAM-A has been reported to facilitate tissue infiltration of leukocytes under inflammatory conditions, the contributions of leukocyte-expressed JAM-A in vivo remain unresolved. We investigated the role of leukocyte-expressed JAM-A in acute peritonitis induced by zymosan, lipopolysaccharide (LPS), or TNFα using mice with selective loss of JAM-A in myelomonocytic cells (LysM-Cre;Jam-afl/fl). Surprisingly, in LysM-Cre;Jam-afl/fl mice, loss of JAM-A did not affect neutrophil (PMN) recruitment into the peritoneum in response to zymosan, LPS, or TNFα although it was significantly reduced in Jam-aKO mice. In parallel, Jam-aKO peritoneal macrophages exhibited diminished CXCL1 chemokine production and decreased activation of NF-kB, whereas those from LysM-Cre;Jam-afl/fl mice were unaffected. Using Villin-Cre;</dcterms:abstract>
   <dcterms:dateAccepted>2025-01-30T14:51:11Z</dcterms:dateAccepted>
   <dcterms:available>2025-01-30T14:51:11Z</dcterms:available>
   <dcterms:created>2025-01-30T14:51:11Z</dcterms:created>
   <dcterms:issued>2019</dcterms:issued>
   <dc:type>journal article</dc:type>
   <dc:identifier>https://hdl.handle.net/20.500.14352/117343</dc:identifier>
   <dc:identifier>XXXX-XXXX</dc:identifier>
   <dc:identifier>10.1038/s41385-019-0143-7</dc:identifier>
   <dc:language>eng</dc:language>
   <dc:relation>1R01DK097256</dc:relation>
   <dc:relation>DK59888</dc:relation>
   <dc:relation>DK55679</dc:relation>
   <dc:relation>DK072564</dc:relation>
   <dc:relation>DK061379</dc:relation>
   <dc:relation>DK079392</dc:relation>
   <dc:relation>Luissint, AC., Williams, H.C., Kim, W. et al. Macrophage-dependent neutrophil recruitment is impaired under conditions of increased intestinal permeability in JAM-A-deficient mice. Mucosal Immunol 12, 668–678 (2019). https://doi.org/10.1038/s41385-019-0143-7</dc:relation>
   <dc:rights>http://creativecommons.org/licenses/by-nc-nd/4.0/</dc:rights>
   <dc:rights>open access</dc:rights>
   <dc:rights>Attribution-NonCommercial-NoDerivatives 4.0 International</dc:rights>
   <dc:publisher>Springer Nature</dc:publisher>
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