{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["207(11)"],"submitter":["Me R"],"pubmed_abstract":["The IL-36 cytokines are known to play various roles in mediating the immune response to infection in a tissue- and pathogen-dependent manner. The present study seeks to investigate the role of IL-36R signaling in C57BL/6 mouse corneas in response to Pseudomonas aeruginosa infection. IL-36α-/-, IL-36γ-/-, and IL-36R-/- mice had significantly more severe keratitis than wild-type mice. At six hours postinfection, IL-36α pretreatment augmented P. aeruginosa-induced expression of IL-1Ra, IL-36γ, LCN2, and S100A8/A9. At one day postinfection, exogenous IL-36α suppressed, whereas IL-36α deficiency promoted, the expression of IL-1β. At three days postinfection, exogenous IL-36α suppressed Th1 but promoted Th2 immune response. IL-36α stimulated the infiltration of IL-22-expressing immune cells, and"],"journal":["Journal of immunology (Baltimore, Md. : 1950)"],"pagination":["2868-2877"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8612993"],"repository":["biostudies-literature"],"pubmed_title":["IL-36α Enhances Host Defense against Pseudomonas aeruginosa Keratitis in C57BL/6 Mouse Corneas."],"pmcid":["PMC8612993"],"pubmed_authors":["Lee PSY","Gao N","Zhang Y","Standiford TJ","Mi QS","Liu T","Wang J","Yu FX","Me R"],"additional_accession":[]},"is_claimable":false,"name":"IL-36α Enhances Host Defense against Pseudomonas aeruginosa Keratitis in C57BL/6 Mouse Corneas.","description":"The IL-36 cytokines are known to play various roles in mediating the immune response to infection in a tissue- and pathogen-dependent manner. The present study seeks to investigate the role of IL-36R signaling in C57BL/6 mouse corneas in response to Pseudomonas aeruginosa infection. IL-36α-/-, IL-36γ-/-, and IL-36R-/- mice had significantly more severe keratitis than wild-type mice. At six hours postinfection, IL-36α pretreatment augmented P. aeruginosa-induced expression of IL-1Ra, IL-36γ, LCN2, and S100A8/A9. At one day postinfection, exogenous IL-36α suppressed, whereas IL-36α deficiency promoted, the expression of IL-1β. At three days postinfection, exogenous IL-36α suppressed Th1 but promoted Th2 immune response. IL-36α stimulated the infiltration of IL-22-expressing immune cells, and","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Dec","modification":"2025-04-25T20:49:14.108Z","creation":"2025-04-06T08:35:10.128Z"},"accession":"S-EPMC8612993","cross_references":{"pubmed":["34686582"],"doi":["10.4049/jimmunol.2001246"]}}