BMC pulmonary medicine · 2025
Exosomes from Tregs mitigate lung damage caused by smoking via inhibiting inflammation and altering T lymphocyte subsets in COPD rats.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Tao Xuefang, Tian Hai, Wang Guowen, Sun Yongzhen, Zhao Liangyan
Аннотация
BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a common disease with respiratory symptoms and limited airflow. Exosomes derived from Tregs (Treg-exo) could regulate immune function and prevent autoimmune disease. This study assessed Treg-exo effects on COPD.
METHODS: In vivo, rats were divided into three groups including control, COPD and exosomes groups. COPD models were established by passive smoking combined with lipopolysaccharide. Phosphate buffered saline or Treg-exo were administered via tail vein. Lung function, Hematoxylin and Eosin staining, and enzyme-linked immunosorbent assay (ELISA) were performed to evaluate lung function, histopathology and inflammation. Flow cytometry was used for peripheral blood T cell separation and counting. In vitro, COPD cluster of differentiation (CD) 4+ T-cells were isolated from spleen and co-cultured with Treg-exo alone or in combination with Colivelin (a signal transducer and activator of transcription 3/STAT3 activator). Flow cytometry, ELISA, and Western blot were used to count T helper cell 17 (Th17) and detected cytokines and STAT3 proteins expression.
RESULTS: In vivo, pulmonary function tests and HE staining showed Treg-exo treatment enhanced lung function and alleviated lung damage; flow cytometry showed Treg-exo treatment decreased CD8+, CD4+ CD25- cells and Th17; ELISA assay found Treg-exo treatment increased transforming growth factor-β and interleukin (IL)-10 and decreased tumor necrosis factor-α and IL-8 in serum, broncho alveolar lavage fluid, and lung tissue. In vitro, Treg-exo treatment inhibited Th17 differentiation and suppressed the content of IL-6, IL-17, and IL-23 and STAT3 phosphorylation.
CONCLUSIONS: Treg-exo suppressed inflammation and CD4+ T-cell differentiation to Th17, possibly by inhibiting STAT3 phosphorylation.
METHODS: In vivo, rats were divided into three groups including control, COPD and exosomes groups. COPD models were established by passive smoking combined with lipopolysaccharide. Phosphate buffered saline or Treg-exo were administered via tail vein. Lung function, Hematoxylin and Eosin staining, and enzyme-linked immunosorbent assay (ELISA) were performed to evaluate lung function, histopathology and inflammation. Flow cytometry was used for peripheral blood T cell separation and counting. In vitro, COPD cluster of differentiation (CD) 4+ T-cells were isolated from spleen and co-cultured with Treg-exo alone or in combination with Colivelin (a signal transducer and activator of transcription 3/STAT3 activator). Flow cytometry, ELISA, and Western blot were used to count T helper cell 17 (Th17) and detected cytokines and STAT3 proteins expression.
RESULTS: In vivo, pulmonary function tests and HE staining showed Treg-exo treatment enhanced lung function and alleviated lung damage; flow cytometry showed Treg-exo treatment decreased CD8+, CD4+ CD25- cells and Th17; ELISA assay found Treg-exo treatment increased transforming growth factor-β and interleukin (IL)-10 and decreased tumor necrosis factor-α and IL-8 in serum, broncho alveolar lavage fluid, and lung tissue. In vitro, Treg-exo treatment inhibited Th17 differentiation and suppressed the content of IL-6, IL-17, and IL-23 and STAT3 phosphorylation.
CONCLUSIONS: Treg-exo suppressed inflammation and CD4+ T-cell differentiation to Th17, possibly by inhibiting STAT3 phosphorylation.