ACTA2 AS1/miR 2278 axis modulates inflammation and epithelial barrier integrity in pediatric Mycoplasma pneumoniae...

Mycoplasma pneumoniae pneumonia (MPP) represents the most common cause of community-acquired pneumonia in Chinese children, where delayed pathogen detection and inadequate severity assessment frequently result in delayed intervention. Given that lncRNA ACTA2-AS1 is markedly downregulated in MP-infected epithelial cells and bioinformatics predicted to sponge miR-2278, this study investigated the molecular mechanism by which lncRNA ACTA2-AS1 regulates inflammatory response and epithelial barrier function via miR-2278, aiming to identify novel targets for precise MPP treatment.

ACTA2-AS1 and miR-2278 expression was quantified in serum and bronchoalveolar lavage fluid (BALF) from 152 MPP children and 106 healthy controls. The clinical utility of ACTA2-AS1 for diagnosing pediatric MPP and predicting severe disease was assessed. BEAS-2B and THP-1 cells were stimulated with lipid-associated membrane protein (LAMP) to establish MPP cell model. The targeting relationship and regulatory effects between ACTA2-AS1 and miR-2278 were validated by co-transfection and dual-luciferase reporter assays.

ACTA2-AS1 was significantly lower in serum and BALF from MPP children, whereas miR-2278 was markedly higher, and the two were negatively correlated. ACTA2-AS1 demonstrated strong diagnostic performance for MPP. Low serum ACTA2-AS1 was associated with abnormal clinical indicators and independently predicted severe MPP. ACTA2-AS1 was confirmed to directly target miR-2278. In vitro, ACTA2-AS1 overexpression enhanced epithelial barrier repair and attenuated inflammation in BEAS-2B and THP-1 cells, while miR-2278 overexpression reversed these protective effects.

ACTA2-AS1 represents a potential biomarker for diagnosing and stratifying MPP children. By sponging miR-2278, it preserves epithelial barrier integrity and modulates immune-inflammatory homeostasis, thereby attenuating MPP progression.