肺炎支原体的致病机制及对大环内酯类抗菌药物耐药机制的研究进展  

Research progress on pathogenic mechanism and drug resistance to macrolide antibiotics of Mycoplasma pneumoniae

作　　者：胡明晰 彭荣(综述) 龚倩(审校) HU Mingxi;PENG Rong;GONG Qian(Department of Clinical Laboratory,Qingpu Branch of Zhongshan Hospital Affiliated to Fudan University,Shanghai 201700,China)

机构地区：[1]复旦大学附属中山医院青浦分院检验科,上海201700

出　　处：《检验医学与临床》2024年第S01期154-158,共5页Laboratory Medicine and Clinic

摘　　要：肺炎支原体(MP)是社区获得性及医院获得性感染常见病原体,耐大环内酯类MP的患病率正在增加,这使治疗变得复杂化。MP的致病机制主要通过对呼吸道上皮细胞的黏附、激活宿主免疫系统以及直接入侵宿主细胞等引起损伤,是一个极其复杂的过程。大环内酯类抗菌药物耐药机制主要集中在23SrRNA和核糖体蛋白的突变上,由于儿科患者的二级治疗选择非常有限,耐药机制的研究将为抗菌药物改造、疫苗、靶向药物的研发提供理论基础,在大环内酯类药物中寻找潜在的新治疗策略,并研究是否存在新的耐药机制。本文综述了MP的致病机制以及对大环内酯类抗菌药物耐药机制的研究进展,为有效预防和治疗肺炎支原体感染,以减少耐药情况的发生,从而提高儿童MP感染的临床疗效。Mycoplasma pneumoniae(MP)is a common pathogen of community-acquired and hospital-acquired infections,but the prevalence of MP resistant macrolides is increasing,which complicates treatment.The pathogenesis of MP is a very complicated process,which mainly causes damage through adhesion to respiratory epithelial cells,activation of host immune system and direct invasion of host cells.The mechanism of resistance to macrolide antibiotics mainly focuses on mutations in 23SrRNA and ribosomal proteins.As secondary treatment options for pediatric patients are very limited,the study of the mechanism of resistance will provide a theoretical basis for the development of antimicrobial modification,vaccines and targeted drugs,search for potential new therapeutic strategies in macrolide drugs,and study whether new resistance mechanisms exist.This article reviewed the pathogenesis of MP and the research progress of resistance mechanism of macrolide antibiotics,in order to effectively prevent and treat mycoplasma pneumoniae infection,reduce the occurrence of drug resistance,and improve the clinical efficacy of MP infection in children.

关 键 词：肺炎支原体 致病机制 大环内酯类抗菌药物 耐药机制 

分 类 号：R446.5[医药卫生—诊断学]