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miR‐182‐5p contributes to intestinal injury in a murine model of Staphylococcus aureus pneumonia‐induced sepsis via targeting surfactant protein D
Author(s) -
Du Xianjin,
Wei Jie,
Tian Dan,
Wu Miao,
Yan Chen,
Hu Peng,
Wu Xu,
Yang Wenbin,
Yin Tailang
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.28995
Subject(s) - apoptosis , sepsis , pneumonia , tumor necrosis factor alpha , inflammation , immune system , biology , immunology , tunel assay , staphylococcus aureus , oncogene , microbiology and biotechnology , downregulation and upregulation , cancer research , medicine , bacteria , gene , cell cycle , biochemistry , genetics
Sepsis is a severe clinical disease, which is resulted from the excessive host inflammation response to the infection. Growing evidence indicates that Staphylococcus aureus pneumonia is a significant cause of sepsis, which can lead to intestinal injury, inflammation, and apoptosis. Studies have shown that miR‐182‐5p can serve as a tumor oncogene or a tumor suppressive microRNA in various cancers, however, its biological role in sepsis is still uninvestigated. Here, we reported that miR‐182‐5p was obviously increased in S. aureus pneumonia mice models. Loss of miR‐182‐5p inhibited intestinal damage and intestinal apoptosis as indicated by the terminal deoxynucleotidyl transferase dUTP nick end labeling assay. In addition, we observed the lack of miR‐182‐5p altered the local inflammatory response to pneumonia in the intestine. Elevated tumor necrosis factor‐α (TNF‐α) and interleukin‐6 (IL‐6) levels were observed in intestinal tissue of pneumonia groups compared with the shams. Furthermore, miR‐182‐5p knockout (KO) pneumonia group demonstrated decreased levels of intestinal TNF‐α and IL‐6. Primary murine intestinal epithelial cells were isolated and cultured in our investigation. We exhibited downregulation of miR‐182‐5p repressed intestinal epithelial cells apoptosis and rescued the cell viability. Meanwhile, miR‐182‐5p caused elevated cell apoptosis and reduced cell proliferation. Moreover, the surfactant protein D (SP‐D) binds with the bacterial pathogens and remove the pathogens and apoptotic bodies, which exhibits important roles in modulating immune responses. It was displayed in our study that SP‐D was greatly decreased in pneumonia mice models. SP‐D was predicted as a downstream target of miR‐182‐5p. These data concluded that miR‐182‐5p promoted intestinal injury in S. aureus pneumonia‐induced sepsis via targeting SP‐D.