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Adenovirus-mediated Over-Expression of FcγRIIB Attenuates Pulmonary Inflammation and Fibrosis.
Zhang, Zhe; Cao, Zhujie; Hou, Lin; Song, Meiyue; Zhou, Yitian; Chen, Yiling; Hu, Huiyuan; Hou, Yangfeng; Liu, Ying; Li, Bolun; Song, Xiaomin; Ge, Weipeng; Li, Baicun; Jiang, Xuehan; Yang, Jie; Song, Dingyun; Zhang, Xinri; Pang, Junling; Zhang, Tiantian; Zhang, Hong; Yang, Peiran; Wang, Jing; Wang, Chen.
  • Zhang Z; First Hospital of Shanxi Medical University, 105862, Department of Pulmonary and Critical Care Medicine, Taiyuan, Shanxi , China.
  • Cao Z; Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Basic Medical Sciences, 196536, Department of Pathophysiology, Beijing, China.
  • Hou L; Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Basic Medical Sciences, 196536, Department of Pathophysiology, Beijing, China.
  • Song M; Chinese Academy of Medical Sciences & Peking Union Medical College, 12501, State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Beijing, China.
  • Zhou Y; Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Basic Medical Sciences, 196536, Department of Pathophysiology, Beijing, China.
  • Chen Y; The First Affiliated Hospital of Xi'an Jiao tong University, Department of Pulmonary and Critical Care Medicine, Xi'an, China.
  • Hu H; The First Affiliated Hospital of Xi'an Jiao tong University, Department of Pulmonary and Critical Care Medicine, Xi'an, China.
  • Hou Y; Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Basic Medical Sciences, 196536, Department of Physiology, Beijing, China.
  • Liu Y; Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Basic Medical Sciences, 196536, Department of Pathophysiology, Beijing, China.
  • Li B; Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Basic Medical Sciences, 196536, Department of Pathophysiology, Beijing, China.
  • Song X; Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Basic Medical Sciences, 196536, Department of Pathophysiology, Beijing, China.
  • Ge W; Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Basic Medical Sciences, 196536, Department of Pathophysiology, Beijing, China.
  • Li B; Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Basic Medical Sciences, 196536, Department of Physiology, Beijing, China.
  • Jiang X; Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Basic Medical Sciences, 196536, Department of Physiology, Beijing, China.
  • Yang J; Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Basic Medical Sciences, 196536, Department of Physiology, Beijing, China.
  • Song D; China-Japan Friendship Hospital, 36635, Department of Pulmonary and Critical Care Medicine, Beijing, China.
  • Zhang X; First Hospital of Shanxi Medical University, 105862, Department of Respiration, Taiyuan, Shanxi , China.
  • Pang J; Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Basic Medical Sciences, 196536, Department of Physiology, Beijing, China.
  • Zhang T; Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Basic Medical Sciences, 196536, Department of Physiology, Beijing, China.
  • Zhang H; Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Basic Medical Sciences, 196536, Department of Pathophysiology, Beijing, China.
  • Yang P; Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Basic Medical Sciences, 196536, Department of Physiology, Beijing, China.
  • Wang J; Chinese Academy of Medical Sciences and Peking Union Medical College Institute of Basic Medical Sciences, 196536, Department of Pathophysiology, Beijing, China; wangjing@ibms.pumc.edu.cn.
  • Wang C; Chinese Academy of Medical Sciences and Peking Union Medical College, 12501, Beijing, China.
Am J Respir Cell Mol Biol ; 2022 Oct 13.
Article in English | MEDLINE | ID: covidwho-2237558
ABSTRACT
Progressive fibrosing interstitial lung diseases (PF-ILDs) result in high mortality and lack effective therapies. The pathogenesis of PF-ILDs involves macrophages driving inflammation and irreversible fibrosis. Fc-gamma receptors (FcγRs) regulate macrophages and inflammation, but their roles in PF-ILDs remain unclear. We characterized the expression of FcγRs and found up-regulated FcγRIIB in human and mouse lungs following exposure to silica. FcγRIIB deficiency aggravated lung dysfunction, inflammation and fibrosis in silica-exposed mice. Using single-cell transcriptomics and in vitro experiments, FcγRIIB was found in alveolar macrophages, where it regulated the expression of fibrosis-related genes Spp1 and Ctss. In mice with macrophage-specific over-expression of FcγRIIB, and in mice treated with adenovirus by intra-tracheal instillation to up-regulate FcγRIIB, silica-induced functional and histological changes were ameliorated. Our data from three genetic models and a therapeutic model suggest that FcγRIIB plays a protective role that can be enhanced by adenoviral over-expression, representing a potential therapeutic strategy for PF-ILDs.
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Full text: Available Collection: International databases Database: MEDLINE Language: English Journal subject: Molecular Biology Year: 2022 Document Type: Article Affiliation country: Rcmb.2022-0056OC

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Full text: Available Collection: International databases Database: MEDLINE Language: English Journal subject: Molecular Biology Year: 2022 Document Type: Article Affiliation country: Rcmb.2022-0056OC