Attenuated lncRNA NKILA Enhances the Secretory Function of Airway Epithelial Cells Stimulated by Mycoplasma pneumoniae via NF-κB.

Fengxia Zhang,Yun Guo,Deyu Zhao,Jiamin Zhang,Feng Liu,Yao Zhou,Haiyan Gu,Qingning Duan,Yifan Zhu,Yanming Xu

doi:10.1155/2021/6656298

Abstract

The secretory function of airway epithelial cells is important in the pathogenesis of Mycoplasma pneumoniae pneumonia (MPP). To investigate the regulatory function of NKILA (nuclear factor-κB (NF-κB) interacting long noncoding RNA (lncRNA)) in MPP, we first detected NKILA as well as the concentration of interleukin 8 (IL-8) and tumor necrosis factor-α (TNF-α) in bronchoalveolar lavage fluid of children with MPP. Then, NKILA was knocked down in epithelial cells to investigate its effect on their secretory function. The results suggested that NKILA was downregulated in children with MPP, while IL-8 and TNF-α levels increased. Knockdown of NKILA in vitro promoted the inflammatory effects of Mycoplasma pneumoniae (MP) in epithelial A549 and BEAS-2B cells. Knockdown of NKILA promoted inhibitor of κBα (IκBα) phosphorylation and degradation, and NF-κB p65 nuclear translocation. Furthermore, RNA immunoprecipitation showed that NKILA could physically bind to IκBα in MP-treated A549 cells. Collectively, our data demonstrated that attenuation of NKILA enhances the effects of MP-stimulated secretory functions of epithelial cells via regulation of NF-κB signaling.

Highlights

Mycoplasma pneumoniae (MP) is a major cause of community-acquired pneumonia, especially in children and young adults [1]
We aimed to investigate the potential role of NKILA in airway inflammation of children with Mycoplasma pneumoniae pneumonia (MPP) and the effect of NKILA on the secretory function of airway epithelial cells in vitro
The results demonstrated that NKILA mRNA was significantly decreased in BALF of the MPP group compared to the ones of the control group (Figure 1(a))

Summary

Introduction

Mycoplasma pneumoniae (MP) is a major cause of community-acquired pneumonia, especially in children and young adults [1]. Accumulating evidence demonstrated that excessive airway inflammation plays an essential role in the development of Mycoplasma pneumoniae pneumonia (MPP) [3,4,5]. When activated by external stimuli such as infection, they release a variety of cytokines, playing a key role in airway inflammation [6]. Cytokine secretion is a complex process, in which nuclear factor-κB (NF-κB), an important inflammatory signaling pathway component, plays pivotal roles [8]. The lipoprotein components of MP can recognize toll-like receptors and activate NF-κB to regulate the secretion of various inflammatory mediators and chemokines, generating airway inflammation [9]. Interleukin 8 (IL-8) and tumor necrosis factor-α

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