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Because nematode migration damages lungs, we speculated that lung-derived damage-associated molecular patterns (DAMPs) possess an IL-33-inducing activity (IL33ia). Indeed, intra-nasal administration of a lung extract induced IL-33 production in lungs. Additionally, lung extracts increased Il33 mRNA expression in primary lung fibroblasts. Proteomic analysis identified retinoblastoma-binding protein 9 (RBBP9) as a major DAMP with IL33ia. RBBP9 was originally discovered as a protein that provides cells with resistance to the growth inhibitory effect of transforming growth factor (TGF)-\u03b21. Here, we found that stimulation by RBBP9 induced primary fibroblasts to produce prostaglandin E2 (PGE2) that, in turn, induced fibroblasts to produce IL-33. RBBP9-activated fibroblasts expressed mRNAs of cyclooxygenase-2 (COX-2) and PGE2 synthase-1 that convert arachidonic acid to PGE2. Furthermore, they expressed PGE2 receptors E-prostanoid (EP) 2 and EP4. Thus, treatment with a COX-2 inhibitor or EP2 and\/or EP4 receptor antagonists inhibited RBBP9-induced IL-33 production. Nematode infection induced pulmonary Il33 mRNA expression, which was inhibited by the COX-2 inhibitor or EP2 and EP4 antagonists, suggesting that nematode infection induced pulmonary Il33 mRNA via PGE2. RBBP9 was expressed constitutively in the lung in the steady state, which did not increase after nematode infection. Finally, we found that Rbbp9-deficient mice had a significantly diminished capacity to increase pulmonary Il33 mRNA expression following nematode infection. Thus, the PGE2-EP2\/EP4 pathway activated by RBBP9 released from damaged lungs is important for pulmonary IL-33 production in nematode-infected animals.<\/jats:p>","DOI":"10.1093\/intimm\/dxaa031","type":"journal-article","created":{"date-parts":[[2020,5,16]],"date-time":"2020-05-16T13:04:07Z","timestamp":1589634247000},"page":"637-652","source":"Crossref","is-referenced-by-count":8,"title":["Lung fibroblasts produce IL-33 in response to stimulation with retinoblastoma-binding protein 9 via production of prostaglandin E2"],"prefix":"10.1093","volume":"32","author":[{"given":"Takumi","family":"Adachi","sequence":"first","affiliation":[{"name":"Department of Immunology, Hyogo College of Medicine , Nishinomiya, Hyogo, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Koubun","family":"Yasuda","sequence":"additional","affiliation":[{"name":"Department of Immunology, Hyogo College of Medicine , Nishinomiya, Hyogo, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Taichiro","family":"Muto","sequence":"additional","affiliation":[{"name":"Department of Immunology, Hyogo College of Medicine , Nishinomiya, Hyogo, Japan"},{"name":"Department of Pediatrics, Aichi Medical University , Nagakute, Aichi, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Satoshi","family":"Serada","sequence":"additional","affiliation":[{"name":"Laboratory of Immune Signal, National Institutes of Biomedical Innovation, Health and Nutrition , Ibaraki, Osaka, Japan"},{"name":"Center for Intractable Immune Disease, Kochi Medical School, Kochi University , Nankoku, Kochi, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tomohiro","family":"Yoshimoto","sequence":"additional","affiliation":[{"name":"Department of Immunology, Hyogo College of Medicine , Nishinomiya, Hyogo, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6728-3872","authenticated-orcid":false,"given":"Ken J","family":"Ishii","sequence":"additional","affiliation":[{"name":"Division of Vaccine Science, Department of Microbiology and Immunology, The Institute of Medical Science, University of Tokyo , Tokyo, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Etsushi","family":"Kuroda","sequence":"additional","affiliation":[{"name":"Department of Immunology, Hyogo College of Medicine , Nishinomiya, Hyogo, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kimi","family":"Araki","sequence":"additional","affiliation":[{"name":"Institute of Resource Development and Analysis, Kumamoto University , Kumamoto, Kumamoto, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masaki","family":"Ohmuraya","sequence":"additional","affiliation":[{"name":"Department of Genetics, Hyogo College of Medicine , Nishinomiya, Hyogo, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tetsuji","family":"Naka","sequence":"additional","affiliation":[{"name":"Laboratory of Immune Signal, National Institutes of Biomedical Innovation, Health and Nutrition , Ibaraki, Osaka, Japan"},{"name":"Center for Intractable Immune Disease, Kochi Medical School, Kochi University , Nankoku, Kochi, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kenji","family":"Nakanishi","sequence":"additional","affiliation":[{"name":"Department of Immunology, Hyogo College of Medicine , Nishinomiya, Hyogo, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2020,6,3]]},"reference":[{"key":"2022070911172656300_CIT0001","doi-asserted-by":"crossref","first-page":"282","DOI":"10.1073\/pnas.0606854104","article-title":"IL-33, the IL-1-like cytokine ligand for ST2 receptor, is a chromatin-associated nuclear factor in vivo","volume":"104","author":"Carriere","year":"2007","journal-title":"Proc. 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