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Interleukin-34 induces pulmonary inflammation in a murine model of lipopolysaccharide-induced acute lung injury
https://showa.repo.nii.ac.jp/records/3856
https://showa.repo.nii.ac.jp/records/38567f9b40d7-3037-4a46-a4b4-f858c28f617a
名前 / ファイル | ライセンス | アクション |
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S33_124.pdf (1.6 MB)
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Item type | 学内発行雑誌 / Departmental Bulletin Paper(1) | |||||
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公開日 | 2022-01-11 | |||||
タイトル | ||||||
タイトル | Interleukin-34 induces pulmonary inflammation in a murine model of lipopolysaccharide-induced acute lung injury | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ | departmental bulletin paper | |||||
著者 |
EBATO, Takaya
× EBATO, Takaya× OHTA, Shin× YAMAGUCHI, Munehiro× MIKUNI, Hatsuko× IKEDA, Hitoshi× JINNO, Megumi× HIRAI, Kuniaki× MIYATA, Yoshito× INOUE, Hideki× HOMMA, Tetsuya× YAMAMOTO, Mayumi× SUZUKI, Shintaro× TANAKA, Akihiko× SAGARA, Hironori |
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書誌情報 |
The Showa University journal of medical sciences 巻 33, 号 4, p. 124-132, 発行日 2021-12 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | 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. C57BL/6 male mice were stimulated intratracheally with lipopolysaccharide (LPS) and sacrificed on day 1, 3, 5, or 7. Additionally, the mice were treated with an anti-IL-34 antibody intranasally before LPS stimulation. 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 cultured with LPS in vitro. The total cell number in BALF was higher in the LPS-stimulated mice than in the control mice. The BALF IL-34 level was significantly elevated in BALF on days 1 and 3. IL-34 expression was detected in the pulmonary epithelium in the LPS-stimulated mice on day 1. Anti-IL-34 antibody suppressed the number of macrophages in BALF. IL-34 blockade resulted in pulmonary fibrosis reduction in LPS-stimulated mice on day 5. LPS stimulation in vitro induced the production of tumor necrosis 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. | |||||
DOI | ||||||
関連識別子 | 10.15369/sujms.33.124 | |||||
出版者 | ||||||
出版者 | Showa University Society | |||||
ISSN | ||||||
収録物識別子 | 2185-0968 | |||||
著者版フラグ | ||||||
出版タイプ | VoR |