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M2 Macrophages Induced Lung Fibrosis Through Expression of IL-34 in Mouse Lung Injured Model
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A2970 - M2 Macrophages Induced Lung Fibrosis Through Expression of IL-34 in Mouse Lung Injured Model
Author Block: H. Mikuni, M. Yamaguchi, T. Kawahara, R. Manabe, N. Kuwahara, M. Jinno, Y. Miyata, K. Hirai, T. Homma, S. Ota, H. Inoue, S. Kusumoto, F. Yamaguchi, M. Yamamoto, S. Suzuki, A. Tanaka, T. Onishi, H. Sagara; Division of Allergology and Respiratory Medicine,School of Medicine,Showa University, Tokyo, Japan.
Abstract:
Rationale: IL-34 was recent discovered cytokine and is known ligand that binds to CSF-1 receptor, thereby enhancing tissue macrophage maturation and differentiation. Expression of IL-34 in the lung was evident, but the localization and the expressing cells were not so far unclear. Also, M2 macrophages are known to play critical role in fibrotic disorders such as NAFLD (Non-alcoholic fatty liver disease). Therefore, we hypothesized that lung epithelial cells derived IL-34 was released and may influence lung fibrosis via M2 macrophage induction. Methods: C57/BL6 Wt mice (8-12 wk-old males) were exposed LPS intratracheally on day 0 and mice were sacrificed on day 1, 3, 5, 7. Bronchoalveolar lavage (BAL) fluid, blood serum and lung tissue were collected . BAL fluid was analyzed for total and differential cell counts. Protein levels of cytokines within BAL fluid and lung tissue were measured by ELISA. Expression and localization of IL-34 in lung tissues were deteced with immunohistochemistry (IHC). Furthermore, M2 macrophages in lung tissue was analyzed by qPCR. In addition, mice were received anti-IL-34 antibody intratracheally for three days before the LPS exposure. THP-1 cells and Beas-2b cells were co-cultured with medium in vitro and Supernatant and cells were collected for expression of cytokines using ELISA and qPCR. Results: IL-34 expression of lung tissue and BAL was increased on day 1 and was detected in lung epithelium in the LPS treated mice. Anti IL-34 antibody suppressed lung inflammation and M2 macrophages differentiation in lung injury mouse model. LPS stimulated THP-1 cells released TNF-alpha and furthermore TNF-alpha stimulated Beas-2b cells inducing IL-34. Also, IL-34 altered M0 macrophages to M2 macrophages using in vitro model. Conclusions: Induction of epithelial cells derived IL-34 may enhance lung fibrosis via M2 macrophages alteration in lung injury mouse model.
Author Block: H. Mikuni, M. Yamaguchi, T. Kawahara, R. Manabe, N. Kuwahara, M. Jinno, Y. Miyata, K. Hirai, T. Homma, S. Ota, H. Inoue, S. Kusumoto, F. Yamaguchi, M. Yamamoto, S. Suzuki, A. Tanaka, T. Onishi, H. Sagara; Division of Allergology and Respiratory Medicine,School of Medicine,Showa University, Tokyo, Japan.
Abstract:
Rationale: IL-34 was recent discovered cytokine and is known ligand that binds to CSF-1 receptor, thereby enhancing tissue macrophage maturation and differentiation. Expression of IL-34 in the lung was evident, but the localization and the expressing cells were not so far unclear. Also, M2 macrophages are known to play critical role in fibrotic disorders such as NAFLD (Non-alcoholic fatty liver disease). Therefore, we hypothesized that lung epithelial cells derived IL-34 was released and may influence lung fibrosis via M2 macrophage induction. Methods: C57/BL6 Wt mice (8-12 wk-old males) were exposed LPS intratracheally on day 0 and mice were sacrificed on day 1, 3, 5, 7. Bronchoalveolar lavage (BAL) fluid, blood serum and lung tissue were collected . BAL fluid was analyzed for total and differential cell counts. Protein levels of cytokines within BAL fluid and lung tissue were measured by ELISA. Expression and localization of IL-34 in lung tissues were deteced with immunohistochemistry (IHC). Furthermore, M2 macrophages in lung tissue was analyzed by qPCR. In addition, mice were received anti-IL-34 antibody intratracheally for three days before the LPS exposure. THP-1 cells and Beas-2b cells were co-cultured with medium in vitro and Supernatant and cells were collected for expression of cytokines using ELISA and qPCR. Results: IL-34 expression of lung tissue and BAL was increased on day 1 and was detected in lung epithelium in the LPS treated mice. Anti IL-34 antibody suppressed lung inflammation and M2 macrophages differentiation in lung injury mouse model. LPS stimulated THP-1 cells released TNF-alpha and furthermore TNF-alpha stimulated Beas-2b cells inducing IL-34. Also, IL-34 altered M0 macrophages to M2 macrophages using in vitro model. Conclusions: Induction of epithelial cells derived IL-34 may enhance lung fibrosis via M2 macrophages alteration in lung injury mouse model.
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