Bone marrow mesenchymal stromal cells attenuate smoke inhalation injury by regulating the M1/M2-Th17/Treg immune homeostasis axis
•Proinflammatory macrophages and Th17 cells mediate acute lung injury in smoke inhalation injury (SII).•MSCs ameliorate lung inflammatory injury by affecting M1/M2 and Th17/Treg immune homeostasis in SII.•MSCs regulate the M1/M2-Th17/Treg immune homeostasis axis via alveolar macrophage-derived IL-23...
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| Veröffentlicht in: | International immunopharmacology 2024-11, Vol.141, p.112986, Article 112986 |
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| creator | Guo, Xiaoqin Niu, Zhifang Zhuang, Yong Zhao, Yunlong Ding, Ziling Shi, Jie Hou, Shike Fan, Haojun Lv, Qi |
| description | •Proinflammatory macrophages and Th17 cells mediate acute lung injury in smoke inhalation injury (SII).•MSCs ameliorate lung inflammatory injury by affecting M1/M2 and Th17/Treg immune homeostasis in SII.•MSCs regulate the M1/M2-Th17/Treg immune homeostasis axis via alveolar macrophage-derived IL-23.
Smoke inhalation injury (SII) is the leading cause of death in fire burn patients. The inflammatory response induced by smoke inhalation is a significant factor in the development of acute lung injury or acute respiratory distress syndrome (ALI/ARDS). Mesenchymal stem cells (MSCs) can alleviate various inflammatory diseases by regulating the polarization of macrophages from the M1 to the M2 phenotype. Moreover, MSCs can facilitate the inflammatory response by regulating Th17/Treg homeostasis. However, little is known about the associations among MSCs, M1/M2 macrophages and Th17/Treg homeostasis. Therefore, the purpose of this study was to evaluate whether MSCs affect subsequent Th17/Treg differentiation and immune homeostasis by regulating M1/M2 polarization in SII. Our results showed that bone marrow mesenchymal stem cells (BMSCs) ameliorated lung inflammatory injury and fibrosis after SII by affecting the polarization of alveolar macrophages (AMs) from the M1 to the M2 phenotype. Moreover, BMSCs maintain Th17/Treg immune homeostasis by increasing the proportion of Treg cells and decreasing the proportion of Th17 cells. In vitro, we further demonstrated that BMSCs promoted the polarization of AMs from the M1 to the M2 phenotype and decreased IL-23 levels. Reduced IL-23 decreased Th17 differentiation and promoted Th17/Treg balance. Therefore, BMSCs ameliorate the inflammatory response and lung damage after SII through regulating M1/M2 polarization and subsequent Th17/Treg immune homeostasis, which are linked to alveolar macrophage-derived IL-23. These findings provide novel insight into how BMSCs regulate the M1/M2-Th17/Treg immune homeostasis axis and provide new therapeutic targets for more effective control of the inflammatory response after SII. |
| doi_str_mv | 10.1016/j.intimp.2024.112986 |
| format | Article |
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Smoke inhalation injury (SII) is the leading cause of death in fire burn patients. The inflammatory response induced by smoke inhalation is a significant factor in the development of acute lung injury or acute respiratory distress syndrome (ALI/ARDS). Mesenchymal stem cells (MSCs) can alleviate various inflammatory diseases by regulating the polarization of macrophages from the M1 to the M2 phenotype. Moreover, MSCs can facilitate the inflammatory response by regulating Th17/Treg homeostasis. However, little is known about the associations among MSCs, M1/M2 macrophages and Th17/Treg homeostasis. Therefore, the purpose of this study was to evaluate whether MSCs affect subsequent Th17/Treg differentiation and immune homeostasis by regulating M1/M2 polarization in SII. Our results showed that bone marrow mesenchymal stem cells (BMSCs) ameliorated lung inflammatory injury and fibrosis after SII by affecting the polarization of alveolar macrophages (AMs) from the M1 to the M2 phenotype. Moreover, BMSCs maintain Th17/Treg immune homeostasis by increasing the proportion of Treg cells and decreasing the proportion of Th17 cells. In vitro, we further demonstrated that BMSCs promoted the polarization of AMs from the M1 to the M2 phenotype and decreased IL-23 levels. Reduced IL-23 decreased Th17 differentiation and promoted Th17/Treg balance. Therefore, BMSCs ameliorate the inflammatory response and lung damage after SII through regulating M1/M2 polarization and subsequent Th17/Treg immune homeostasis, which are linked to alveolar macrophage-derived IL-23. These findings provide novel insight into how BMSCs regulate the M1/M2-Th17/Treg immune homeostasis axis and provide new therapeutic targets for more effective control of the inflammatory response after SII.</description><identifier>ISSN: 1567-5769</identifier><identifier>ISSN: 1878-1705</identifier><identifier>EISSN: 1878-1705</identifier><identifier>DOI: 10.1016/j.intimp.2024.112986</identifier><identifier>PMID: 39182266</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Alveolar macrophages ; Animals ; Cell Differentiation ; Cells, Cultured ; Homeostasis ; Humans ; Interleukin-23 - metabolism ; Lung - immunology ; Lung - pathology ; M1/M2 ; Macrophages, Alveolar - immunology ; Male ; Mesenchymal Stem Cell Transplantation ; Mesenchymal stem cells ; Mesenchymal Stem Cells - immunology ; Mice ; Mice, Inbred C57BL ; Polarization ; Smoke inhalation injury ; Smoke Inhalation Injury - immunology ; Smoke Inhalation Injury - therapy ; T-Lymphocytes, Regulatory - immunology ; Th17 Cells - immunology ; Th17/Treg</subject><ispartof>International immunopharmacology, 2024-11, Vol.141, p.112986, Article 112986</ispartof><rights>2024</rights><rights>Copyright © 2024. Published by Elsevier B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c241t-3c9417140b4a28cc376edc4ca5b03c5e60c8ef0e4bee4d075730d25c530e9ce33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1567576924015078$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39182266$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guo, Xiaoqin</creatorcontrib><creatorcontrib>Niu, Zhifang</creatorcontrib><creatorcontrib>Zhuang, Yong</creatorcontrib><creatorcontrib>Zhao, Yunlong</creatorcontrib><creatorcontrib>Ding, Ziling</creatorcontrib><creatorcontrib>Shi, Jie</creatorcontrib><creatorcontrib>Hou, Shike</creatorcontrib><creatorcontrib>Fan, Haojun</creatorcontrib><creatorcontrib>Lv, Qi</creatorcontrib><title>Bone marrow mesenchymal stromal cells attenuate smoke inhalation injury by regulating the M1/M2-Th17/Treg immune homeostasis axis</title><title>International immunopharmacology</title><addtitle>Int Immunopharmacol</addtitle><description>•Proinflammatory macrophages and Th17 cells mediate acute lung injury in smoke inhalation injury (SII).•MSCs ameliorate lung inflammatory injury by affecting M1/M2 and Th17/Treg immune homeostasis in SII.•MSCs regulate the M1/M2-Th17/Treg immune homeostasis axis via alveolar macrophage-derived IL-23.
Smoke inhalation injury (SII) is the leading cause of death in fire burn patients. The inflammatory response induced by smoke inhalation is a significant factor in the development of acute lung injury or acute respiratory distress syndrome (ALI/ARDS). Mesenchymal stem cells (MSCs) can alleviate various inflammatory diseases by regulating the polarization of macrophages from the M1 to the M2 phenotype. Moreover, MSCs can facilitate the inflammatory response by regulating Th17/Treg homeostasis. However, little is known about the associations among MSCs, M1/M2 macrophages and Th17/Treg homeostasis. Therefore, the purpose of this study was to evaluate whether MSCs affect subsequent Th17/Treg differentiation and immune homeostasis by regulating M1/M2 polarization in SII. Our results showed that bone marrow mesenchymal stem cells (BMSCs) ameliorated lung inflammatory injury and fibrosis after SII by affecting the polarization of alveolar macrophages (AMs) from the M1 to the M2 phenotype. Moreover, BMSCs maintain Th17/Treg immune homeostasis by increasing the proportion of Treg cells and decreasing the proportion of Th17 cells. In vitro, we further demonstrated that BMSCs promoted the polarization of AMs from the M1 to the M2 phenotype and decreased IL-23 levels. Reduced IL-23 decreased Th17 differentiation and promoted Th17/Treg balance. Therefore, BMSCs ameliorate the inflammatory response and lung damage after SII through regulating M1/M2 polarization and subsequent Th17/Treg immune homeostasis, which are linked to alveolar macrophage-derived IL-23. These findings provide novel insight into how BMSCs regulate the M1/M2-Th17/Treg immune homeostasis axis and provide new therapeutic targets for more effective control of the inflammatory response after SII.</description><subject>Alveolar macrophages</subject><subject>Animals</subject><subject>Cell Differentiation</subject><subject>Cells, Cultured</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Interleukin-23 - metabolism</subject><subject>Lung - immunology</subject><subject>Lung - pathology</subject><subject>M1/M2</subject><subject>Macrophages, Alveolar - immunology</subject><subject>Male</subject><subject>Mesenchymal Stem Cell Transplantation</subject><subject>Mesenchymal stem cells</subject><subject>Mesenchymal Stem Cells - immunology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Polarization</subject><subject>Smoke inhalation injury</subject><subject>Smoke Inhalation Injury - immunology</subject><subject>Smoke Inhalation Injury - therapy</subject><subject>T-Lymphocytes, Regulatory - immunology</subject><subject>Th17 Cells - immunology</subject><subject>Th17/Treg</subject><issn>1567-5769</issn><issn>1878-1705</issn><issn>1878-1705</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE9v1DAQxS0EoqXlGyDkI5fs-m-cXJCggoLUisv2bDnObOMljhfbAfbYb15HKRx7mqeZN_M0P4TeUbKhhNbbw8ZN2fnjhhEmNpSytqlfoHPaqKaiisiXRctaVVLV7Rl6k9KBkNIX9DU64y1tGKvrc_TwOUyAvYkx_MEeEkx2OHkz4pRjWKqFcUzY5AzTbDLg5MNPwG4azGiyC1ORhzmecHfCEe7npTnd4zwAvqXbW1btBqq2uzLCzvu5ZA3BQ0jZJFfO_nXpEr3amzHB26d6ge6-ftldfatuflx_v_p0U1kmaK64bQVVVJBOGNZYy1UNvRXWyI5wK6EmtoE9AdEBiJ4oqTjpmbSSE2gtcH6BPqx3jzH8miFl7V1avjMThDlpTlpFZSHbFKtYrTaGlCLs9TG6wuikKdELfH3QK3y9wNcr_LL2_ilh7jz0_5f-0S6Gj6sByp-_HUSdrCvEoXcRbNZ9cM8nPAKbYpme</recordid><startdate>20241115</startdate><enddate>20241115</enddate><creator>Guo, Xiaoqin</creator><creator>Niu, Zhifang</creator><creator>Zhuang, Yong</creator><creator>Zhao, Yunlong</creator><creator>Ding, Ziling</creator><creator>Shi, Jie</creator><creator>Hou, Shike</creator><creator>Fan, Haojun</creator><creator>Lv, Qi</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20241115</creationdate><title>Bone marrow mesenchymal stromal cells attenuate smoke inhalation injury by regulating the M1/M2-Th17/Treg immune homeostasis axis</title><author>Guo, Xiaoqin ; Niu, Zhifang ; Zhuang, Yong ; Zhao, Yunlong ; Ding, Ziling ; Shi, Jie ; Hou, Shike ; Fan, Haojun ; Lv, Qi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c241t-3c9417140b4a28cc376edc4ca5b03c5e60c8ef0e4bee4d075730d25c530e9ce33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Alveolar macrophages</topic><topic>Animals</topic><topic>Cell Differentiation</topic><topic>Cells, Cultured</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Interleukin-23 - metabolism</topic><topic>Lung - immunology</topic><topic>Lung - pathology</topic><topic>M1/M2</topic><topic>Macrophages, Alveolar - immunology</topic><topic>Male</topic><topic>Mesenchymal Stem Cell Transplantation</topic><topic>Mesenchymal stem cells</topic><topic>Mesenchymal Stem Cells - immunology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Polarization</topic><topic>Smoke inhalation injury</topic><topic>Smoke Inhalation Injury - immunology</topic><topic>Smoke Inhalation Injury - therapy</topic><topic>T-Lymphocytes, Regulatory - immunology</topic><topic>Th17 Cells - immunology</topic><topic>Th17/Treg</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guo, Xiaoqin</creatorcontrib><creatorcontrib>Niu, Zhifang</creatorcontrib><creatorcontrib>Zhuang, Yong</creatorcontrib><creatorcontrib>Zhao, Yunlong</creatorcontrib><creatorcontrib>Ding, Ziling</creatorcontrib><creatorcontrib>Shi, Jie</creatorcontrib><creatorcontrib>Hou, Shike</creatorcontrib><creatorcontrib>Fan, Haojun</creatorcontrib><creatorcontrib>Lv, Qi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>International immunopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guo, Xiaoqin</au><au>Niu, Zhifang</au><au>Zhuang, Yong</au><au>Zhao, Yunlong</au><au>Ding, Ziling</au><au>Shi, Jie</au><au>Hou, Shike</au><au>Fan, Haojun</au><au>Lv, Qi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bone marrow mesenchymal stromal cells attenuate smoke inhalation injury by regulating the M1/M2-Th17/Treg immune homeostasis axis</atitle><jtitle>International immunopharmacology</jtitle><addtitle>Int Immunopharmacol</addtitle><date>2024-11-15</date><risdate>2024</risdate><volume>141</volume><spage>112986</spage><pages>112986-</pages><artnum>112986</artnum><issn>1567-5769</issn><issn>1878-1705</issn><eissn>1878-1705</eissn><abstract>•Proinflammatory macrophages and Th17 cells mediate acute lung injury in smoke inhalation injury (SII).•MSCs ameliorate lung inflammatory injury by affecting M1/M2 and Th17/Treg immune homeostasis in SII.•MSCs regulate the M1/M2-Th17/Treg immune homeostasis axis via alveolar macrophage-derived IL-23.
Smoke inhalation injury (SII) is the leading cause of death in fire burn patients. The inflammatory response induced by smoke inhalation is a significant factor in the development of acute lung injury or acute respiratory distress syndrome (ALI/ARDS). Mesenchymal stem cells (MSCs) can alleviate various inflammatory diseases by regulating the polarization of macrophages from the M1 to the M2 phenotype. Moreover, MSCs can facilitate the inflammatory response by regulating Th17/Treg homeostasis. However, little is known about the associations among MSCs, M1/M2 macrophages and Th17/Treg homeostasis. Therefore, the purpose of this study was to evaluate whether MSCs affect subsequent Th17/Treg differentiation and immune homeostasis by regulating M1/M2 polarization in SII. Our results showed that bone marrow mesenchymal stem cells (BMSCs) ameliorated lung inflammatory injury and fibrosis after SII by affecting the polarization of alveolar macrophages (AMs) from the M1 to the M2 phenotype. Moreover, BMSCs maintain Th17/Treg immune homeostasis by increasing the proportion of Treg cells and decreasing the proportion of Th17 cells. In vitro, we further demonstrated that BMSCs promoted the polarization of AMs from the M1 to the M2 phenotype and decreased IL-23 levels. Reduced IL-23 decreased Th17 differentiation and promoted Th17/Treg balance. Therefore, BMSCs ameliorate the inflammatory response and lung damage after SII through regulating M1/M2 polarization and subsequent Th17/Treg immune homeostasis, which are linked to alveolar macrophage-derived IL-23. These findings provide novel insight into how BMSCs regulate the M1/M2-Th17/Treg immune homeostasis axis and provide new therapeutic targets for more effective control of the inflammatory response after SII.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>39182266</pmid><doi>10.1016/j.intimp.2024.112986</doi></addata></record> |
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| subjects | Alveolar macrophages Animals Cell Differentiation Cells, Cultured Homeostasis Humans Interleukin-23 - metabolism Lung - immunology Lung - pathology M1/M2 Macrophages, Alveolar - immunology Male Mesenchymal Stem Cell Transplantation Mesenchymal stem cells Mesenchymal Stem Cells - immunology Mice Mice, Inbred C57BL Polarization Smoke inhalation injury Smoke Inhalation Injury - immunology Smoke Inhalation Injury - therapy T-Lymphocytes, Regulatory - immunology Th17 Cells - immunology Th17/Treg |
| title | Bone marrow mesenchymal stromal cells attenuate smoke inhalation injury by regulating the M1/M2-Th17/Treg immune homeostasis axis |
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