IL-17 stimulates neutrophils to release S100A8/A9 to promote lung epithelial cell apoptosis in Mycoplasma pneumoniae–induced pneumonia in children - 09/10/21
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Abstract |
Mycoplasma pneumoniae-induced pneumonia (MPP) is a common cause of community-acquired respiratory tract infections, increasing risk of morbidity and mortality, in children. However, diagnosing early-stage MPP is difficult owing to the lack of good diagnostic methods. Here, we examined the protein profile of bronchoalveolar lavage fluid (BALF) and found that S100A8/A9 was highly expressed. Enzyme-linked immunosorbent assays used to assess protein levels in serum samples indicated that S100A8/A9 concentrations were also increased in serum obtained from children with MPP, with no change in S100A8/A9 levels in children with viral or bacterial pneumonia. In vitro, S100A8/A9 treatment significantly increased apoptosis in a human alveolar basal epithelial cell line (A549 cells). Bioinformatics analyses indicated that up-regulated S100A8/A9 proteins participated in the interleukin (IL)−17 signaling pathway. The origin of the increased S100A8/A9 was investigated in A549 cells and in neutrophils obtained from children with MPP. Treatment of neutrophils, but not of A549 cells, with IL-17A released S100A8/A9 into the culture medium. In summary, we demonstrated that S100A8/A9, possibly released from neutrophils, is a new potential biomarker for the clinical diagnosis of children MPP and involved in the development of this disease through enhancing apoptosis of alveolar basal epithelial cells.
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Highlights |
• | S100A8/A9 are increased in the serum and BALF of children with MPP. |
• | S100A8/A9 enhance the apoptosis of human alveolar basal epithelial cells. |
• | IL-17A can stimulate neutrophils to release S100A8/A9. |
Keywords : Mycoplasma pneumoniae pneumonia, S100A8/S100A9, Lung epithelial cell, Apoptosis, IL-17
Plan
Vol 143
Article 112184- novembre 2021 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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