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<dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:invenio="http://invenio-software.org/elements/1.0" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"><dc:identifier>doi:10.1177/2050640617727180</dc:identifier><dc:language>eng</dc:language><dc:creator>Latorre, E.</dc:creator><dc:creator>Layunta, E.</dc:creator><dc:creator>Grasa, L.</dc:creator><dc:creator>Pardo, J.</dc:creator><dc:creator>García, S.</dc:creator><dc:creator>Alcalde, A. I.</dc:creator><dc:creator>Mesonero, J. E.</dc:creator><dc:title>Toll-like receptors 2 and 4 modulate intestinal IL-10 differently in ileum and colon</dc:title><dc:identifier>ART-2018-102262</dc:identifier><dc:description>Background: Inflammatory bowel diseases are consequence of an intestinal homeostasis breakdown in which innate immune dysregulation is implicated. Toll-like receptor (TLR)2 and TLR4 are immune recognition receptors expressed in the intestinal epithelium, the first physical-physiological barrier for microorganisms, to inform the host of the presence of Gram-positive and Gram-negative organisms. Interleukin (IL)-10 is an essential anti-inflammatory cytokine that contributes to maintenance of intestinal homeostasis. Aim: Our main aim was to investigate intestinal IL-10 synthesis and release, and whether TLR2 and TLR4 are determinants of IL-10 expression in the intestinal tract. Methods: We used Caco-2 cell line as an enterocyte-like cell model, and also ileum and colon from mice deficient in TLR2, TLR4 or TLR2/4 to test the involvement of TLR signaling. Results: Intestinal epithelial cells are able to synthesize and release IL-10 and their expression is increased after TLR2 or TLR4 activation. IL-10 regulation seems to be tissue specific, with IL-10 expression in the ileum regulated by a compensation between TLR2 and TLR4 expression, whereas in the colon, TLR2 and TLR4 affect IL-10 expression independently. Conclusions: Intestinal epithelial cells could release IL-10 in response to TLR activation, playing an intestinal tissue-dependent and critical intestinal immune role.</dc:description><dc:date>2018</dc:date><dc:source>http://zaguan.unizar.es/record/69935</dc:source><dc:doi>10.1177/2050640617727180</dc:doi><dc:identifier>http://zaguan.unizar.es/record/69935</dc:identifier><dc:identifier>oai:zaguan.unizar.es:69935</dc:identifier><dc:relation>info:eu-repo/grantAgreement/ES/DGA/B61</dc:relation><dc:relation>info:eu-repo/grantAgreement/ES/MICINN-FEDER/BFU2010-18971</dc:relation><dc:relation>info:eu-repo/grantAgreement/ES/UZ/2014-BIO-03</dc:relation><dc:identifier.citation>United European Gastroenterology Journal 6, 3 (2018), 446-453</dc:identifier.citation><dc:rights>All rights reserved</dc:rights><dc:rights>http://www.europeana.eu/rights/rr-f/</dc:rights><dc:rights>info:eu-repo/semantics/openAccess</dc:rights></dc:dc>

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