肺炎支原体参与支气管哮喘发病机制的研究进展

Progress on mycoplasma pneumoniae in the pathogenesis of asthma

肺炎支原体(mycoplasma pneumoniae,MP)感染及支气管哮喘为儿童常见的呼吸系统疾病,二者密切相关。MP感染诱发支气管哮喘发作,抗MP感染治疗对支气管哮喘患儿病情的控制有一定的帮助。该文阐述MP参与支气管哮喘发病机制,为哮喘的治疗提供理论依据。MP感染可损伤气道上皮导致感染后咳嗽,甚至诱发支气管哮喘发作;MP感染气道上皮后分泌社区获得性呼吸窘迫综合征毒素(community-acquired respiratory distress syndrome toxin,CARDS Tx)与气道黏膜结合造成气道上皮损伤,同时参与TH2介导的免疫反应,介导特异性IgE的产生,进而诱导炎症介质释放;MP感染后释放的炎症因子增加,同时导致呼出气一氧化氮(fractional exhaled nitric oxide,FeNO)升高,加重气道高反应及气道重塑。治疗方面,大环内酯类药物治疗MP感染的同时,可对气道产生抗炎及免疫调节作用,可降低激素依赖性哮喘患儿所需的激素剂量,减少哮喘发作的次数并延长哮喘患儿缓解期。

Mycoplasma pneumoniae(MP)infection and asthma are common respiratory diseases in children,and they are closely related.MP infection induces asthma attacks,and anti-MP infection treatment can help control the degree in children with asthma.This article describes the relationship between MP infection and asthma,and provides a theoretical basis for the treatment of asthma.MP infection can damage the airway and cause chronic cough and bronchial asthma attacks.MP infects the airway epithelium and secretes community-acquired respiratory distress syndrome toxin(CARDS Tx)combined with the airway mucosa to cause the airway epithelial damage,and promotes the body to form a TH2-mediated immune response,mediates the production of specific IgE,and then triggers the release of inflammatory mediators involved in asthma;the increase of inflammatory factors released after MP infection will also cause exhaled breath.Fractional exhaled nitric oxide(FeNO)is elevated,which can lead to airway hyperresponsiveness and airway remodeling.In view of treatment,when treating MP infections with macrolide drugs,they can also have anti-inflammatory and immunomodulatory effects on the airways,which can reduce the steroid dose required by children with steroid-dependent asthma,reduce the frequency of asthma attacks and prolong remission period in children with asthma.