Brain, behavior, and immunity · 2025
Social defeat stress aggravates asthma airway inflammation through neutrophils.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
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Deng Huan, Huang Xia, Zhang Jiamin, Zhu Beibei, Bao Yaqing, Miao Xueqing, Jiang Xinyi, Du Yi, Li Huilin, Zhao Deyu, Guo Yun, Liu Feng
Аннотация
BACKGROUNDS: Psychological stress is a recognized contributor to asthma progression and is associated with increased neutrophils.
OBJECTIVE: To investigate the role of neutrophils and NETosis in psychosocial stress aggravates asthma airway inflammation.
METHODS: We constructed murine asthma models under social defeat stress (SDS) intervention. Wild-type,Csf3-deficient (Csf3-/-, neutropenic), andPadi4-deficient (Padi4-/-, impaired NETosis) mice were used to explore neutrophil-driven mechanisms.
RESULTS: In murine asthma models, SDS exacerbated airway hyperresponsiveness, inflammation, and remodeling. The amplified effects of SDS were attenuated in Csf3-/- mice with neutropenia but exacerbated in neutrophilic mice. Transcriptomic analysis revealed SDS enhanced neutrophil extracellular traps (NETs) formation. Genetic inhibition of NETosis (Padi4-/-) mitigated the SDS-induced asthma hyperresponsiveness and inflammation.
CONCLUSIONS: Neutrophils and NETosis are critical mediators of SDS-induced asthma airway hyperresponsiveness, inflammation and mucus hypersecretion, highlighting potential therapeutic targets.
OBJECTIVE: To investigate the role of neutrophils and NETosis in psychosocial stress aggravates asthma airway inflammation.
METHODS: We constructed murine asthma models under social defeat stress (SDS) intervention. Wild-type,Csf3-deficient (Csf3-/-, neutropenic), andPadi4-deficient (Padi4-/-, impaired NETosis) mice were used to explore neutrophil-driven mechanisms.
RESULTS: In murine asthma models, SDS exacerbated airway hyperresponsiveness, inflammation, and remodeling. The amplified effects of SDS were attenuated in Csf3-/- mice with neutropenia but exacerbated in neutrophilic mice. Transcriptomic analysis revealed SDS enhanced neutrophil extracellular traps (NETs) formation. Genetic inhibition of NETosis (Padi4-/-) mitigated the SDS-induced asthma hyperresponsiveness and inflammation.
CONCLUSIONS: Neutrophils and NETosis are critical mediators of SDS-induced asthma airway hyperresponsiveness, inflammation and mucus hypersecretion, highlighting potential therapeutic targets.