Abstract
Our aim was to determine whether the long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in Mycoplasma pneumoniae pneumonia (MPP), and its possible mechanism of action. MALAT1 expression in the bronchoalveolar lavage fluid of 50 hospitalized children with MPP was compared to its expression in 30 children with intrabronchial foreign bodies. MALAT1 expression was higher in children with MPP, accompanied by increased inflammatory mediators interleukin 8 (IL-8) and tumor necrosis factor alpha (TNF-α), compared to the controls. In human airway epithelial cells infected with wild-type Mycoplasma pneumoniae (strain M129), MALAT1, IL-8, and TNF-α expression significantly increased, and increased expression of IL-8 and TNF-α could be suppressed by MALAT1 knockdown. Luciferase reporter gene assay and western blot showed that knockdown of MALAT1 reduced nuclear factor-κB (NF-κB) activation. In vivo, RNAi packaged with adenovirus (Adv) was nasally transfected into BALB/c mice to silence MALAT1, and an MP-infected mouse pneumonia model was prepared. The results demonstrated that the degree of pulmonary inflammatory injury, vascular permeability, secretion of inflammatory factors, and expression of phosphorylated p65 (pp65) in MP-infected mice were partly reversed after MALAT1 knockdown compared to those in the controls. In conclusion, MALAT1 is involved in the regulation of airway and pulmonary inflammation caused by MP infection via NF-κB regulation.
Highlights
Mycoplasma pneumoniae (MP) is one of the main causes of community-acquired pneumonia in children (Jain et al, 2015)
The results demonstrated that levels of interleukin 8 (IL-8) and TNF-α secreted by A549 and BEAS2B cells were increased after MP infection compared to the control group, while the inflammatory cytokines levels decreased in Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1)-depleted epithelial cells compared to those of the non-knockdown group after MP infection (Figures 2B,C,E,F, all P < 0.05)
The results showed that both the mRNA and protein expression of IL-8 and TNF-α in the shNC + MP group significantly increased compared to the shNC + PBS group, FIGURE 5 | MALAT1 knockdown reduced lung injury in BALB/c mice caused by MP infection. (A,B) The shNC + MP group mice exhibited increases in protein concentration in lung homogenate and ratio of protein concentration in lung homogenate and serum compared to the shNC+PBS group
Summary
Mycoplasma pneumoniae (MP) is one of the main causes of community-acquired pneumonia in children (Jain et al, 2015). Pneumonia caused by MP often leads to serious complications that affect the quality of life in children (Zhang et al, 2016). In patients with Mycoplasma pneumoniae pneumonia (MPP), excessive inflammatory response is a leading cause of pulmonary inflammation and is predictive of poor prognosis. The mechanism that leads to the uncontrolled inflammatory response in MPP is still unclear, and further investigation is necessary. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), one of the first lncRNAs associated with human disease to be identified, is of interest because it is widely evolutionarily conserved. MALAT1 was originally identified as a prognostic marker for poor clinical prognosis
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