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

Authors

Xiaoya Li, Yanru Mi, Qinmei Lu, Congzhe Li

Published in

Annals of agricultural and environmental medicine : AAEM. Volume 33. Issue 3. Pages 385-392. Sep 21, 2026. Epub Feb 03, 2026.

Abstract

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.
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.
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.
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.

PMID:
42802960
Bibliographic data and abstract were imported from PubMed on 28 Sep 2026.

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