The Protective Effect of Naringenin on Airway Remodeling after Mycoplasma Pneumoniae Infection by Inhibiting Autophagy-Mediated Lung Inflammation and Fibrosis.

Yan Lin,Zhen Xiao,Qianna Kan,Zhiyan Jiang,Dan Tan

doi:10.1155/2018/8753894

Abstract

Our previous study has shown that Chinese medicine, Qingfei Tongluo formula (QTF), has a significantly therapeutic effect to Mycoplasma pneumoniae (MP) pneumonia (MPP). The aim of this study was to investigate the therapeutic effect and mechanism of naringenin (NRG) on MPP which was an important component of QTF. Here, we studied 124 children with or without MPP and compared inflammatory cytokines and fibrinogen-related protein expression with enzyme-linked immunosorbent assay. We also employed a BALB/c mouse model of MPP and divided the mice into three groups: ctrl (normal control mice), MPP (MP-infected mice), and MPP + NRG (MP-infected mice treated with NRG). BEAS-2B cells were used to confirm the relationship between autophagy, inflammation, and fibrosis. The results show proinflammatory cytokines (interleukin- [IL-] 6, IL-1β, and tumor necrosis factor-α), and transforming growth factor beta (TGF-β) expression was significantly increased after MP infection from both clinical and animal experiment. In vivo experimental confirmation showed that NRG treatment decreased MPP-induced lung injury in mice by inhibiting autophagy-mediated inflammatory cytokine expression and pulmonary fibrosis. In vitro experiments confirmed it. These results indicate that NRG treatment suppressed the inflammatory response and pulmonary fibrosis by inhibition of autophagy after MP infection.

Highlights

Mycoplasma pneumoniae (MP) is a common cause of community-acquired pneumonia, mainly in children and young adults, and is well known to cause a wide variety of respiratory and extrapulmonary diseases [1, 2]
The results show that children with MP pneumonia have a higher ratio of neutrophils and white blood cells in whole blood cell analysis
This suggests that MP infection can induce the inflammatory response

Summary

Introduction

Mycoplasma pneumoniae (MP) is a common cause of community-acquired pneumonia, mainly in children and young adults, and is well known to cause a wide variety of respiratory and extrapulmonary diseases [1, 2]. Increasing evidence has confirmed that the symptoms of pneumonia caused by MP are correlated with the induction of proinflammatory cytokine expression and pulmonary fibrosis [3,4,5]. MP infection can lead to proinflammatory cytokine, tumor necrosis factor-α (TNF-α), and chemokines, such as interleukin- (IL-) 6, promoting the recruitment of various leukocytes, primarily neutrophils, to the site of infection, eventually leading to lung injury and pulmonary fibrosis. A conserved eukaryotic stress-response pathway in which cells sequester damaged or surplus proteins and organelles in double-membrane vesicles and deliver them to lysosomes for degradation, plays a seminal role in antimicrobial host defense. Autophagy is strongly induced by bacteria, viruses, and fungal organisms that are enclosed within autophagosomes and digested within the autophagolysosomes [7, 8]. The relationship between MP-induced autophagy and inflammatory responses remains unknown

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