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作 者:Qiang Zhou Meiyu Chang Ning Li Yi Guan Sanqiao Yao
机构地区:[1]School of Public Health,North China University of Science and Technology,Tangshan 063000,Hebei,China [2]School of Public Health,Xinxiang Medical University,Xinxiang 453003,Henan,China
出 处:《Biomedical and Environmental Sciences》2025年第4期469-483,共15页生物医学与环境科学(英文版)
基 金:supported by the National Natural Science Foundation of China Joint Fund for Regional Innovation and Development(Grant numbers [U21A20334]);the Postgraduate Innovation Funding Project of Hebei Province(Grant numbers [CXZZBS2022116])。
摘 要:Objective Recent studies have overturned the traditional concept of the lung as a “sterile organ” revealing that pulmonary microbiota dysbiosis and abnormal surfactant proteins(SPs) expression are involved in the progression of silicosis. This study aimed to investigate the relationship between abnormal SPs expression and dysbiosis of lung microbiota in silica-induced lung fibrosis, providing insights into mechanisms of silicosis.Methods Lung pathology, SPs expression, and microbiota composition were evaluated in silicaexposed mice. A mouse model of antibiotic-induced microbiota depletion was established, and alveolar structure and SPs expression were assessed. The roles of the lung microbiota and SPs in silicosis progression were further evaluated in mice with antibiotic-induced microbiota depletion, both with and without silica exposure.Results Silica exposure induced lung inflammation and fibrosis, along with increased expression of SPA expression. Antibiotics(Abx)-induced microbiota depletion elevated SP-A and SP-D expression.Furthermore, silica exposure altered lung microbiota composition, enriching potentially pathogenic taxa.However, antibiotic-induced microbiota depletion prior to silica exposure reduced silica-mediated lung fibrosis and inflammation.Conclusion Lung microbiota is associated with silica-induced lung injury. Overproduction of SP-A and SP-D, induced by Abx-induced microbiota depletion, may enhance the resistance of mouse lung tissue to silica-induced injury.
关 键 词:16s rRNA sequencing FIBROSIS Lung microbiota ANTIBIOTICS Surfactant proteins
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