Yaxing Shen1,2, Jieqiong Song3, Yingqin Wang3, Zhenglong Chen4, Lin Zhang5, Jie Yu3, Duming Zhu3, Ming Zhong3. 1. Department of Thoracic Surgery, Zhongshan Hospital Fudan University, Shanghai 200032, China. 2. Department of Thoracic Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China. 3. Department of Critical Care Medicine, Zhongshan Hospital Fudan University, Shanghai 200032, China. 4. School of Medical Instrumentation, Shanghai University of Medicine & Health Sciences, Shanghai 201318, China. 5. Center of Emergency and Intensive Care Unit, Jinshan Hospital Fudan University, Shanghai 201508, China.
Abstract
BACKGROUND: Macrophages can polarize to M2 phenotype to decrease inflammation and encourage tissue repair. Nonetheless, its role in sepsis-induced acute lung injury and its effect on endothelial cells (ECs) regeneration remains unknown. The aim of the current study was to explore the impact of M2 macrophages on pulmonary ECs proliferation in sepsis-induced acute lung injury. METHODS: We co-cultured mouse lung microvascular endothelial cells (MLMVECs) with M2 macrophages following LPS challenge. M2 macrophages were intratracheally transplanted into mice subjected to cecal ligation and puncture (CLP). We further performed cytokine array for the supernatant from M2 macrophages and serum from mice subjected with CLP. RESULTS: We found both co-culture with M2 macrophages and treating with supernatant from M2 macrophages increased ECs viability following LPS challenge. Intratracheal transplantation of M2 macrophages markedly promoted pulmonary ECs proliferation, manifesting as attenuation of lung microvascular permeability and lung tissue edema, as well as improvement of survival rate. We further found that CXCL12, IL-1ra, TIMP-1, IL-4, and CXCL1 were increased in the supernatant of M2 macrophages in vitro. G-CSF and Complement Component 5a (C5/C5a) were increased in the serum of the M2-transplanted mice. CONCLUSIONS: The present study suggested M2 macrophages could promote ECs proliferation in sepsis-induced ALI through secretion of anti-inflammatory cytokines and growth factors.
BACKGROUND: Macrophages can polarize to M2 phenotype to decrease inflammation and encourage tissue repair. Nonetheless, its role in sepsis-induced acute lung injury and its effect on endothelial cells (ECs) regeneration remains unknown. The aim of the current study was to explore the impact of M2 macrophages on pulmonary ECs proliferation in sepsis-induced acute lung injury. METHODS: We co-cultured mouse lung microvascular endothelial cells (MLMVECs) with M2 macrophages following LPS challenge. M2 macrophages were intratracheally transplanted into mice subjected to cecal ligation and puncture (CLP). We further performed cytokine array for the supernatant from M2 macrophages and serum from mice subjected with CLP. RESULTS: We found both co-culture with M2 macrophages and treating with supernatant from M2 macrophages increased ECs viability following LPS challenge. Intratracheal transplantation of M2 macrophages markedly promoted pulmonary ECs proliferation, manifesting as attenuation of lung microvascular permeability and lung tissue edema, as well as improvement of survival rate. We further found that CXCL12, IL-1ra, TIMP-1, IL-4, and CXCL1 were increased in the supernatant of M2 macrophages in vitro. G-CSF and Complement Component 5a (C5/C5a) were increased in the serum of the M2-transplanted mice. CONCLUSIONS: The present study suggested M2 macrophages could promote ECs proliferation in sepsis-induced ALI through secretion of anti-inflammatory cytokines and growth factors.
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