{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1363670318839475712.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.4049/jimmunol.177.2.1323"}},{"identifier":{"@type":"URI","@value":"https://academic.oup.com/jimmunol/article-pdf/177/2/1323/62643374/zim01406001323.pdf"}}],"dc:title":[{"@value":"Interleukin-13 Enhances Cyclooxygenase-2 Expression in Activated Rat Brain Microglia: Implications for Death of Activated Microglia"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:title>Abstract</jats:title>\n               <jats:p>Brain inflammation has recently attracted widespread interest because it is a risk factor for the onset and progression of brain diseases. In this study, we report that cyclooxygenase-2 (COX-2) plays a key role in the resolution of brain inflammation by inducing the death of microglia. We previously reported that IL-13, an anti-inflammatory cytokine, induced the death of activated microglia. These results revealed that IL-13 significantly enhanced COX-2 expression and production of PGE2 and 15-deoxy-Δ12,14-PGJ2 (15d-PGJ2) in LPS-treated microglia. Two other anti-inflammatory cytokines, IL-10 and TGF-β, neither induced microglial death nor enhanced COX-2 expression or PGE2 or 15d-PGJ2 production. Therefore, we hypothesized that the effect of IL-13 on COX-2 expression may be linked to death of activated microglia. We found that COX-2 inhibitors (celecoxib and NS398) suppressed the death of microglia induced by a combination of LPS and IL-13 and that exogenous addition of PGE2 and 15d-PGJ2 induced microglial death. Agonists of EP2 (butaprost) and peroxisome proliferator-activated receptor γ (ciglitazone) mimicked the effect of PGE2 and 15d-PGJ2, and an EP2 antagonist (AH6809) and a peroxisome proliferator-activated receptor γ antagonist (GW9662) suppressed microglial death induced by LPS in combination with IL-13. In addition, IL-13 potentiated LPS-induced activation of JNK, and the JNK inhibitor SP600125 suppressed the enhancement of COX-2 expression and attenuated microglial death. Taken together, these results suggest that IL-13 enhanced COX-2 expression in LPS-treated microglia through the enhancement of JNK activation. Furthermore, COX-2 products, PGE2 and 15d-PGJ2, caused microglial death, which terminates brain inflammation.</jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1383670318839475584","@type":"Researcher","foaf:name":[{"@value":"Myung-Soon Yang"}],"jpcoar:affiliationName":[{"@value":"Department of Pharmacology, Ajou University School of Medicine , Suwon ,"},{"@value":"Neuroscience Graduate Program, Ajou University School of Medicine , Suwon ,"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670318839475841","@type":"Researcher","foaf:name":[{"@value":"Kyung-Ae Ji"}],"jpcoar:affiliationName":[{"@value":"Department of Pharmacology, Ajou University School of Medicine , Suwon ,"},{"@value":"Neuroscience Graduate Program, Ajou University School of Medicine , Suwon ,"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670318839475712","@type":"Researcher","foaf:name":[{"@value":"Sae-Bom Jeon"}],"jpcoar:affiliationName":[{"@value":"Neuroscience Graduate Program, Ajou University School of Medicine , Suwon ,"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670318839475842","@type":"Researcher","foaf:name":[{"@value":"Byung-Kwan Jin"}],"jpcoar:affiliationName":[{"@value":"Neuroscience Graduate Program, Ajou University School of Medicine , Suwon ,"},{"@value":"Brain Disease Research Center, Ajou University School of Medicine , Suwon ,"}]},{"@id":"https://cir.nii.ac.jp/crid/1380585449892047232","@type":"Researcher","foaf:name":[{"@value":"Seung U Kim"}],"jpcoar:affiliationName":[{"@value":"Neuroscience Graduate Program, Ajou University School of Medicine , Suwon ,"},{"@value":"Brain Disease Research Center, Ajou University School of Medicine , Suwon ,"},{"@value":"Department of Neurology, University of British Columbia , Vancouver ,"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670318839475585","@type":"Researcher","foaf:name":[{"@value":"Ilo Jou"}],"jpcoar:affiliationName":[{"@value":"Department of Pharmacology, Ajou University School of Medicine , Suwon ,"},{"@value":"Chronic Inflammatory Disease Research Center, Ajou University School of Medicine , Suwon ,"}]},{"@id":"https://cir.nii.ac.jp/crid/1383670318839475586","@type":"Researcher","foaf:name":[{"@value":"Eunhye Joe"}],"jpcoar:affiliationName":[{"@value":"Department of Pharmacology, Ajou University School of Medicine , Suwon ,"},{"@value":"Neuroscience Graduate Program, Ajou University School of Medicine , Suwon ,"},{"@value":"Brain Disease Research Center, Ajou University School of Medicine , Suwon ,"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"00221767"},{"@type":"EISSN","@value":"15506606"}],"prism:publicationName":[{"@value":"The Journal of Immunology"}],"dc:publisher":[{"@value":"Oxford University Press (OUP)"}],"prism:publicationDate":"2006-07","prism:volume":"177","prism:number":"2","prism:startingPage":"1323","prism:endingPage":"1329"},"reviewed":"false","dc:rights":["https://academic.oup.com/pages/standard-publication-reuse-rights"],"url":[{"@id":"https://academic.oup.com/jimmunol/article-pdf/177/2/1323/62643374/zim01406001323.pdf"}],"createdAt":"2014-04-18","modifiedAt":"2025-03-29","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1360004232160389888","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Astrocytic mobilization of glutathione peroxidase-1 contributes to the protective potential against cocaine kindling behaviors in mice via activation of JAK2/STAT3 signaling"}]},{"@id":"https://cir.nii.ac.jp/crid/1360285714665905280","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Plexin-A1 is required for Toll-like receptor-mediated microglial activation in the development of lipopolysaccharide-induced encephalopathy"}]},{"@id":"https://cir.nii.ac.jp/crid/1360846645842516352","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Cutting Edge: IL-13Rα1 Expression in Dopaminergic Neurons Contributes to Their Oxidative Stress–Mediated Loss following Chronic Peripheral Treatment with Lipopolysaccharide"}]}],"dataSourceIdentifier":[{"@type":"CROSSREF","@value":"10.4049/jimmunol.177.2.1323"},{"@type":"CROSSREF","@value":"10.1016/j.freeradbiomed.2018.12.027_references_DOI_3bXXsSqI8tnyoiwKnyuZLqCg8FU"},{"@type":"CROSSREF","@value":"10.4049/jimmunol.1102150_references_DOI_3bXXsSqI8tnyoiwKnyuZLqCg8FU"},{"@type":"CROSSREF","@value":"10.3892/ijmm.2014.1690_references_DOI_3bXXsSqI8tnyoiwKnyuZLqCg8FU"}]}