{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhao J"],"funding":["Yunnan Ten Thousand Talents Plan Young and Elite Talents Project","National Natural Science Foundation of China"],"pagination":["66"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11829554"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["21(1)"],"pubmed_abstract":["<h4>Background</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.<h4>Results</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"],"journal":["BMC veterinary research"],"pubmed_title":["Escherichia coli HPI-induced duodenitis through ubiquitin regulation of the TLR4/NF-κB pathway."],"pmcid":["PMC11829554"],"funding_grant_id":["YNWR-CYJS-2018-047","31960692"],"pubmed_authors":["Gao B","Shen J","Cha J","Chen L","Wang H","Gao H","Shan C","Xiao P","Yang W","Zhao R","Xiao J","Wang S","Xin A","Zhao J","Zhang B","Liu G"],"additional_accession":[]},"is_claimable":false,"name":"Escherichia coli HPI-induced duodenitis through ubiquitin regulation of the TLR4/NF-κB pathway.","description":"<h4>Background</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.<h4>Results</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","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Feb","modification":"2026-06-02T04:21:26.291Z","creation":"2025-06-27T03:05:47.075Z"},"accession":"S-EPMC11829554","cross_references":{"pubmed":["39953596"],"doi":["10.1186/s12917-025-04515-3"]}}