MicroRNA‑20a promotes inflammation via the nuclear factor‑κB signaling pathway in pediatric pneumonia

Abstract

Pneumonia is a common respiratory disease worldwide, which is preventable and treatable; however, it is recognized as a leading cause of mortality in children. The present study aimed to investigate the role and mechanism of microRNA (miR)‑20a in inflammation in pediatric pneumonia. Clinical serum samples were collected from children with pneumonia and healthy children. Initially, the serum expression levels of miR‑20a were detected by reverse transcription‑quantitative polymerase chain reaction. Subsequently, A549 cells were randomly divided into four groups: Control group; lipopolysaccharide (LPS; 1 µg/ml) group; LPS + miR‑20a group; and LPS + miR‑20a + pyrrolidine dithiocarbamate (PDTC; 100 mmol/l) group. The concentrations of interleukin‑6 (IL‑6), tumor necrosis factor (TNF)‑α and C‑reactive protein (CRP) in clinical serum samples and A549 cells were determined by ELISA. In addition, the protein expression levels of inhibitor of nuclear factor (NF)‑κB α (IκBα) and phosphorylated (p)‑NF‑κB were measured by western blotting. The results demonstrated that miR‑20a was upregulated in children with pneumonia and in lung cells with LPS‑induced inflammatory injury (P<0.01). In addition, compared with the LPS group, cells in the LPS + miR‑20a group exhibited increased expression levels of IL‑6, TNF‑α and CRP (P<0.05). Overexpression of miR‑20a also resulted in upregulation of the expression levels of IκBα and p‑NF‑κB compared with in the LPS group (P<0.05). Furthermore, treatment with the NF‑κB inhibitor PDTC inhibited the expression of inflammatory factors compared with in the LPS + miR‑20a group (P<0.05). In conclusion, the present study indicated that miR‑20a is upregulated in pediatric pneumonia, and overexpression of miR‑20a may promote inflammation through activation of the NF‑κB signaling pathway.

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

“…The effect of NF‐κB activation on inflammation has been reported in glomerulonephritis, arthritis and other inflammatory disorders . A latest study reported that blocking of the NF‐κB pathway inhibited the expression of inflammatory factors in A549 cells . Overexpression of TBL1XR1 activates the NF‐κB pathway, promoting the transcription of downstream anti‐apoptosis genes .…”

“…36 A number of studies have revealed that the NF-κB pathway involved in the mediation of inflammation, and the activation of NF-κB pathway influence the immune response by up-regulating the secretion of pro-inflammatory cytokines. 37,38 The effect of NF-κB activation on inflammation has been reported in glomerulonephritis, arthritis and other inflammatory disorders. 39,40 A latest study reported that blocking of the NF-κB pathway inhibited the expression of inflammatory factors in A549 cells.…”

LncRNA MALAT1 regulates inflammatory cytokine production in lipopolysaccharide‐stimulated human gingival fibroblasts through sponging miR‐20a and activating TLR4 pathway

“…MiR‐20a locates in human chromosome 13q31‐q32 and is involved in the regulation of inflammatory responses . In human alveolar epithelial cell line A549, LPS stimulation increases the level of miR‐20a, and miR‐20a mimic increases the levels of IL‐6, TNF‐α, C‐reactive protein, IκBα, and p‐NF‐κB .…”

“…12,17,18 Also, lncRNAs may act as the MiR-20a locates in human chromosome 13q31-q32 and is involved in the regulation of inflammatory responses. [19][20][21][22] In human alveolar epithelial cell line A549, LPS stimulation increases the level of miR-20a, and miR-20a mimic increases the levels of IL-6, TNF-α, C-reactive protein, IκBα, and p-NF-κB. 22 From our results, the expression of miR-20a was reduced by LPS stimulation; however, overexpression of miR-20a inhibited the level of TLR4 and inflammatory cytokines IL-6 and IL-8, which is consistent to Philippe et al's research.…”

“…[19][20][21][22] In human alveolar epithelial cell line A549, LPS stimulation increases the level of miR-20a, and miR-20a mimic increases the levels of IL-6, TNF-α, C-reactive protein, IκBα, and p-NF-κB. 22 From our results, the expression of miR-20a was reduced by LPS stimulation; however, overexpression of miR-20a inhibited the level of TLR4 and inflammatory cytokines IL-6 and IL-8, which is consistent to Philippe et al's research. 21 Furthermore, we found that miR-20a inhibits the expression of TLR4 via binding to TLR4 3′-UTR.…”