Exosomal miR-103a-3p ameliorates lipopolysaccharide-induced immune response in BEAS-2B cells via NF-κB pathway by targeting transducin β-like 1X related protein 1.

Abnormal immune response contributes to pathophysiology of pneumonia and is recognized as a main factor for high incidence rate in children. The association between exosomes and inflammation has been reported in diverse cell types and diseases. The current study focuses on exploring the effects of exosomal miR-103a-3p on lipopolysaccharide (LPS)-induced inflammation, and investigates the underlying mechanisms. We proved that miR-103a-3p was lowly expressed in blood samples of pneumonia patients and LPS-induced lung cells, and overexpression of miR-103a-3p weaken the LPS-induced inflammation. Using luciferase reporter assay and immunoprecipitation assay, we demonstrated that miR-103a-3p directly binds to a specific region of transducin β-like 1X related protein 1 (TBL1XR1), mediating the NF-κB signalling pathway, thus regulating immune response. Taken together, our data revealed that miR-103a-3p functions as an anti-inflammatory gene in childhood pneumonia and can be applied as therapeutic targets for the treatment of childhood pneumonia in the future.