Clinical significance of serum ATP8B1 in children with Mycoplasma pneumoniae infection complicated with myocardial injury.

INTRODUCTION AND OBJECTIVE: Mycoplasma pneumoniae (MP) infection can lead to various extrapulmonary complications, including myocardial injury (MI). However, the expression levels of ATPase phospholipid transporting 8B1 (ATP8B1) in MP-infected individuals with MI and its potential therapeutic role remain elusive. The aim of the study is to evaluate ATP8B1 as a therapeutic target for MP-induced MI. MATERIAL AND METHODS: The study quantified ATP8B1 expression in patient serum via RT-qPCR and analyzed its diagnostic value for MP and MP+MI using receiver operating characteristic (ROC) curves. Binary logistic regression assessed its association with MP+MI. Serum interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α) levels were measured by ELISA and correlated with ATP8B1. In a dual-cell model (MP-infected BEAS-2B cells and AC16 cells exposed to their supernatant), ATP8B1's effects on inflammation, proliferation, reactive oxygen species (ROS), and cardiac injury markers were evaluated via RT-qPCR, CCK-8, and ELISA. RESULTS: The study revealed that serum ATP8B1 levels were significantly reduced in the MP group and further decreased in the MP+MI group. ATP8B1 expression levels could distinguish MP patients from MP+MI patients. Serum IL-6 and TNF-α levels were significantly higher in the MP+MI group than in the MP group, and ATP8B1 was negatively correlated with IL-6 and TNF-α. In vitro, ATP8B1 was downregulated in both cell lines. Functionally, over-expression of ATP8B1 effectively attenuated inflammation, ROS production, deficits in cell proliferation, and myocardial injury. CONCLUSIONS: ATP8B1 was expressed lowly in the serum of MP+MI patients. Functional experiments demonstrated that ATP8B1 upregulation significantly attenuated inflammation, ROS generation, proliferation deficits, and myocardial injury.