<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zhao J</submitter><funding>Yunnan Ten Thousand Talents Plan Young and Elite Talents Project</funding><funding>National Natural Science Foundation of China</funding><pagination>66</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11829554</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>21(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>The Highly Pathogenic Island (HPI) found in Yersinia pestis can be horizontally transferred to E. coli, enhancing its virulence and pathogenicity. Ubiquitin (Ub) acts as an activator of the NF-κB pathway and plays a critical role in the inflammatory response. However, the precise mechanism by which Ub and the regulated TLR4/NF-κB pathway contribute to HPI-induced intestinal inflammation in E. coli remains unclear.&lt;h4>Results&lt;/h4>In this study, we established Ub overexpression models of small intestinal epithelial cells (in vitro) and BALB/c mice (in vivo) and infected these models with HPI-rich E. coli. We investigated the role of the Ub-regulated TLR4/NF-κB pathway in E. coli HPI-induced intestinal inflammation through qPCR, ELISA, immunofluorescence, immunohistochemist</pubmed_abstract><journal>BMC veterinary research</journal><pubmed_title>Escherichia coli HPI-induced duodenitis through ubiquitin regulation of the TLR4/NF-κB pathway.</pubmed_title><pmcid>PMC11829554</pmcid><funding_grant_id>YNWR-CYJS-2018-047</funding_grant_id><funding_grant_id>31960692</funding_grant_id><pubmed_authors>Gao B</pubmed_authors><pubmed_authors>Shen J</pubmed_authors><pubmed_authors>Cha J</pubmed_authors><pubmed_authors>Chen L</pubmed_authors><pubmed_authors>Wang H</pubmed_authors><pubmed_authors>Gao H</pubmed_authors><pubmed_authors>Shan C</pubmed_authors><pubmed_authors>Xiao P</pubmed_authors><pubmed_authors>Yang W</pubmed_authors><pubmed_authors>Zhao R</pubmed_authors><pubmed_authors>Xiao J</pubmed_authors><pubmed_authors>Wang S</pubmed_authors><pubmed_authors>Xin A</pubmed_authors><pubmed_authors>Zhao J</pubmed_authors><pubmed_authors>Zhang B</pubmed_authors><pubmed_authors>Liu G</pubmed_authors></additional><is_claimable>false</is_claimable><name>Escherichia coli HPI-induced duodenitis through ubiquitin regulation of the TLR4/NF-κB pathway.</name><description>&lt;h4>Background&lt;/h4>The Highly Pathogenic Island (HPI) found in Yersinia pestis can be horizontally transferred to E. coli, enhancing its virulence and pathogenicity. Ubiquitin (Ub) acts as an activator of the NF-κB pathway and plays a critical role in the inflammatory response. However, the precise mechanism by which Ub and the regulated TLR4/NF-κB pathway contribute to HPI-induced intestinal inflammation in E. coli remains unclear.&lt;h4>Results&lt;/h4>In this study, we established Ub overexpression models of small intestinal epithelial cells (in vitro) and BALB/c mice (in vivo) and infected these models with HPI-rich E. coli. We investigated the role of the Ub-regulated TLR4/NF-κB pathway in E. coli HPI-induced intestinal inflammation through qPCR, ELISA, immunofluorescence, immunohistochemist</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Feb</publication><modification>2026-06-02T04:21:26.291Z</modification><creation>2025-06-27T03:05:47.075Z</creation></dates><accession>S-EPMC11829554</accession><cross_references><pubmed>39953596</pubmed><doi>10.1186/s12917-025-04515-3</doi></cross_references></HashMap>