IL-17 stimulates neutrophils to release S100A8/A9 to promote lung epithelial cell apoptosis in Mycoplasma pneumoniae–induced pneumonia in children

• Published in: Biomedicine & pharmacotherapy 2021-11, Vol.143, p.112184-112184, Article 112184
• Main Authors: Bai, Suwen, Wang, Wang, Ye, Li, Fang, Lulu, Dong, Tao, Zhang, Rong, Wang, Xin, Gao, Huiwen, Shen, Bing, Ding, Shenggang
• Format: Article
• Language: English
• Subjects: A549 Cells; Alveolar Epithelial Cells - immunology; Alveolar Epithelial Cells - metabolism; Alveolar Epithelial Cells - microbiology; Alveolar Epithelial Cells - pathology; Apoptosis; Biomarkers - metabolism; Calgranulin A - metabolism; Calgranulin B - metabolism; Case-Control Studies; Child; Child, Preschool; Female; Host-Pathogen Interactions; Humans; IL-17; Infant; Interleukin-17 - pharmacology; Lung epithelial cell; Male; Mycoplasma pneumoniae - immunology; Mycoplasma pneumoniae - pathogenicity; Mycoplasma pneumoniae pneumonia; Neutrophils - drug effects; Neutrophils - immunology; Neutrophils - metabolism; Neutrophils - microbiology; Paracrine Communication; Pneumonia, Mycoplasma - immunology; Pneumonia, Mycoplasma - metabolism; Pneumonia, Mycoplasma - microbiology; Pneumonia, Mycoplasma - pathology; S100A8/S100A9; Signal Transduction
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/j.biopha.2021.112184

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. [Display omitted] •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.