Downregulation of caspase‑3 alleviates Mycoplasma pneumoniae‑induced apoptosis in alveolar epithelial cells.

Mycoplasma pneumoniae (M. pneumoniae) infection is closely associated with pneumonia in children. Apoptosis of alveolar epithelial cells is involved in the development of pneumonia in children. The present study aimed to examine how caspase‑3 influences apoptosis rates in M. pneumoniae‑infected alveolar epithelial cells. A549 alveolar epithelial cells were treated with M. pneumoniae, and cells and culture supernatant were collected at different time points. Alterations in apoptosis rates and caspase‑3 mRNA and protein levels were measured for each treatment group. Cell apoptosis was detected using flow cytometry and TUNEL assay, and cell proliferation was detected using Cell Counting Kit‑8 assay. Caspase‑3 expression in A549 cells was inhibited via small interfering RNA (siRNA) knockdown and relative alterations in mRNA and protein levels and apoptosis rates were measured. Cytokine levels were measured using ELISA assay. Apoptosis rates of alveolar epithelial cells increased with prolonged exposure to M. pneumoniae (P<0.05). M. pneumoniae infection increased interleukin (IL)‑4, IL‑6 and IL‑13 levels and reduced IL‑10 levels. Caspase‑3 was upregulated, whereas B cell lymphoma (Bcl)‑2 was downregulated upon M. pneumoniae exposure for 24 h (P<0.05). Following 12 and 24 h of treatment, caspase‑3 levels in the siRNA‑treated cells were decreased compared with control group (P<0.05). M. pneumoniae also significantly altered caspase‑3 and Bcl‑2 protein expression. M. pneumoniae promoted apoptosis in alveolar epithelial cells via activation of the external death receptor pathway. Therefore, M. pneumoniae infection may affect the development of pneumonia in children by regulating caspase‑3 expression and promoting apoptosis.