{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yang R"],"funding":["Fundamental Research Funds for the Central Universities","Natural Science Foundation of Hubei Province","China Agricultural Research System","China Postdoctoral Science Foundation","National Natural Science Foundation of China","National Key Research and Development Program of China"],"pagination":["988-999"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10928716"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(3)"],"pubmed_abstract":["<i>Escherichia coli</i> continues to be the predominant Gram-negative pathogen causing neonatal meningitis worldwide. Inflammatory mediators have been implicated in the pathogenesis of meningitis and are key therapeutic targets. The role of interleukin-22 (IL-22) in various diseases is diverse, with both protective and pathogenic effects. However, little is understood about the mechanisms underlying the damaging effects of IL-22 on the blood-brain barrier (BBB) in <i>E. coli</i> meningitis. We observed that meningitic <i>E. coli</i> infection induced IL-22 expression in the serum and brain of mice. The tight junction proteins (TJPs) components ZO-1, Occludin, and Claudin-5 were degraded in the mouse brain and human brain microvascular endothelial cells (hBMEC) following IL-22 administration. Moreover, the meningitic <i>E. coli</i>-caused increase in BBB permeability in wild-type mice was restored by knocking out IL-22. Mechanistically, IL-22 activated the STAT3-VEGFA signaling cascade in <i>E. coli</i> meningitis, thus eliciting the degradation of TJPs to induce BBB disruption. Our data indicated that IL-22 is an essential host accomplice during <i>E. coli</i>-caused BBB disruption and could be targeted for the therapy of bacterial meningitis."],"journal":["ACS infectious diseases"],"pubmed_title":["Interleukin-22 Contributes to Blood-Brain Barrier Disruption via STAT3/VEGFA Activation in <i>Escherichia coli</i> Meningitis."],"pmcid":["PMC10928716"],"funding_grant_id":["2022M721277","2021YFD1800800","2021CFA016","32102749","CARS-35","2662023PY005"],"pubmed_authors":["Liu H","Chen J","Tan C","Yang R","Qu X","Wang X","Chen H"],"additional_accession":[]},"is_claimable":false,"name":"Interleukin-22 Contributes to Blood-Brain Barrier Disruption via STAT3/VEGFA Activation in <i>Escherichia coli</i> Meningitis.","description":"<i>Escherichia coli</i> continues to be the predominant Gram-negative pathogen causing neonatal meningitis worldwide. Inflammatory mediators have been implicated in the pathogenesis of meningitis and are key therapeutic targets. The role of interleukin-22 (IL-22) in various diseases is diverse, with both protective and pathogenic effects. However, little is understood about the mechanisms underlying the damaging effects of IL-22 on the blood-brain barrier (BBB) in <i>E. coli</i> meningitis. We observed that meningitic <i>E. coli</i> infection induced IL-22 expression in the serum and brain of mice. The tight junction proteins (TJPs) components ZO-1, Occludin, and Claudin-5 were degraded in the mouse brain and human brain microvascular endothelial cells (hBMEC) following IL-22 administration. Moreover, the meningitic <i>E. coli</i>-caused increase in BBB permeability in wild-type mice was restored by knocking out IL-22. Mechanistically, IL-22 activated the STAT3-VEGFA signaling cascade in <i>E. coli</i> meningitis, thus eliciting the degradation of TJPs to induce BBB disruption. Our data indicated that IL-22 is an essential host accomplice during <i>E. coli</i>-caused BBB disruption and could be targeted for the therapy of bacterial meningitis.","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Mar","modification":"2025-04-19T05:51:32.022Z","creation":"2025-04-19T05:51:32.022Z"},"accession":"S-EPMC10928716","cross_references":{"pubmed":["38317607"],"doi":["10.1021/acsinfecdis.3c00668"]}}