T. Ebato, S. Ohta, Munehiro Yamaguchi, H. Mikuni, H. Ikeda, M. Jinno, K. Hirai, Y. Miyata, H. Inoue, T. Homma, Mayumi Yamamoto, S. Suzuki, A. Tanaka, H. Sagara
{"title":"Interleukin-34 induces pulmonary inflammation in a murine model of lipopolysaccharide-induced acute lung injury","authors":"T. Ebato, S. Ohta, Munehiro Yamaguchi, H. Mikuni, H. Ikeda, M. Jinno, K. Hirai, Y. Miyata, H. Inoue, T. Homma, Mayumi Yamamoto, S. Suzuki, A. Tanaka, H. Sagara","doi":"10.15369/sujms.33.124","DOIUrl":null,"url":null,"abstract":"The cytokine interleukin-34 ( IL-34 ) was recently described. However, its role in the lungs is not well understood. IL-34 binds to the colony stimulating factor-1 receptor, thereby enhancing tissue macrophage maturation and differentiation. Macrophages are essential to the airway inflammation process and acute lung injury ( ALI ) . This study aimed to evaluate the role of IL-34 in ALI establishment. The bronchoalveolar lavage fluid ( BALF ) and lung tissues were collected. The cells of the human peripheral blood monocyte cell line THP-1 and the human airway epithelial cell line BEAS-2B were with LPS in vitro . The total in the than in the factor- α ( TNF- α) in THP-1 cells. Furthermore, TNF- α stimulation induced the IL-34 production in BEAS-2B cells. These results suggest that IL-34 induction in the epithelial cells may enhance pulmonary inflammation and fibrosis in the murine model of LPS-induced acute lung injury.","PeriodicalId":23019,"journal":{"name":"The Showa University Journal of Medical Sciences","volume":"12 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Showa University Journal of Medical Sciences","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.15369/sujms.33.124","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
The cytokine interleukin-34 ( IL-34 ) was recently described. However, its role in the lungs is not well understood. IL-34 binds to the colony stimulating factor-1 receptor, thereby enhancing tissue macrophage maturation and differentiation. Macrophages are essential to the airway inflammation process and acute lung injury ( ALI ) . This study aimed to evaluate the role of IL-34 in ALI establishment. The bronchoalveolar lavage fluid ( BALF ) and lung tissues were collected. The cells of the human peripheral blood monocyte cell line THP-1 and the human airway epithelial cell line BEAS-2B were with LPS in vitro . The total in the than in the factor- α ( TNF- α) in THP-1 cells. Furthermore, TNF- α stimulation induced the IL-34 production in BEAS-2B cells. These results suggest that IL-34 induction in the epithelial cells may enhance pulmonary inflammation and fibrosis in the murine model of LPS-induced acute lung injury.