<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Polosukhina D</submitter><funding>BLRD VA</funding><funding>Crohn's &amp; Colitis Foundation of America</funding><funding>NIDDK NIH HHS</funding><funding>NCI NIH HHS</funding><funding>NIGMS NIH HHS</funding><funding>CSRD VA</funding><pagination>6540-6546</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8629429</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>40(47)</volume><pubmed_abstract>CCL11, also known as eotaxin-1, is described as an eosinophil chemoattractant, which has been implicated in allergic and Th2 inflammatory diseases. We have reported that CCL11 is significantly increased in the serum of inflammatory bowel disease (IBD) patients, colonic eosinophils are increased and correlate with tissue CCL11 levels in ulcerative colitis patients, and CCL11 is increased in dextran sulfate sodium (DSS)-induced murine colitis. Here, we show that CCL11 is involved in the pathogenesis of DSS-induced colitis and in colon tumorigenesis in the azoxymethane (AOM)-DSS model of colitis-associated carcinogenesis (CAC). Ccl11&lt;sup>-/-&lt;/sup> mice exposed to DSS then allowed to recover had significantly less body weight loss and a decrease in histologic injury versus wild-type (WT) mice.</pubmed_abstract><journal>Oncogene</journal><pubmed_title>CCL11 exacerbates colitis and inflammation-associated colon tumorigenesis.</pubmed_title><pmcid>PMC8629429</pmcid><funding_grant_id>P01 CA028842</funding_grant_id><funding_grant_id>T32 DK007673</funding_grant_id><funding_grant_id>U24 DK059637</funding_grant_id><funding_grant_id>P30 DK058404</funding_grant_id><funding_grant_id>P01 CA116087</funding_grant_id><funding_grant_id>IK2 BX002126</funding_grant_id><funding_grant_id>703003</funding_grant_id><funding_grant_id>R01 DK128200</funding_grant_id><funding_grant_id>P30 CA068485</funding_grant_id><funding_grant_id>T32 GM008554</funding_grant_id><funding_grant_id>I01 BX004366</funding_grant_id><funding_grant_id>P50 CA236733</funding_grant_id><funding_grant_id>I01 CX002171</funding_grant_id><funding_grant_id>R01 CA190612</funding_grant_id><pubmed_authors>Washington MK</pubmed_authors><pubmed_authors>Barry DP</pubmed_authors><pubmed_authors>Asim M</pubmed_authors><pubmed_authors>Singh K</pubmed_authors><pubmed_authors>Hardbower DM</pubmed_authors><pubmed_authors>Coburn LA</pubmed_authors><pubmed_authors>Gobert AP</pubmed_authors><pubmed_authors>Wilson KT</pubmed_authors><pubmed_authors>Piazuelo MB</pubmed_authors><pubmed_authors>Polosukhina D</pubmed_authors><pubmed_authors>Allaman MM</pubmed_authors></additional><is_claimable>false</is_claimable><name>CCL11 exacerbates colitis and inflammation-associated colon tumorigenesis.</name><description>CCL11, also known as eotaxin-1, is described as an eosinophil chemoattractant, which has been implicated in allergic and Th2 inflammatory diseases. We have reported that CCL11 is significantly increased in the serum of inflammatory bowel disease (IBD) patients, colonic eosinophils are increased and correlate with tissue CCL11 levels in ulcerative colitis patients, and CCL11 is increased in dextran sulfate sodium (DSS)-induced murine colitis. Here, we show that CCL11 is involved in the pathogenesis of DSS-induced colitis and in colon tumorigenesis in the azoxymethane (AOM)-DSS model of colitis-associated carcinogenesis (CAC). Ccl11&lt;sup>-/-&lt;/sup> mice exposed to DSS then allowed to recover had significantly less body weight loss and a decrease in histologic injury versus wild-type (WT) mice.</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Nov</publication><modification>2025-04-04T19:57:53.974Z</modification><creation>2025-04-04T19:57:53.974Z</creation></dates><accession>S-EPMC8629429</accession><cross_references><pubmed>34625710</pubmed><doi>10.1038/s41388-021-02046-3</doi></cross_references></HashMap>