A truncated mutation of MucA in Pseudomonas aeruginosa from a bronchiectasis patient affects T3SS expression and inflammasome activation  

作　　者：Yanan Liu Lin Du Yongzhang Zhu Xuefei Liu Ning Zhou Congcong Li Qingtian Li Ping He 

机构地区：[1]Department of Laboratory Medicine,Ruijin Hospital,Shanghai Jiao Tong University School of Medicine,Shanghai 200000,China [2]Department of Medical Microbiology and Parasitology,Shanghai Jiao Tong University School of Medicine,Shanghai 200000,China [3]School of Global Health,Shanghai Jiao Tong Univerisy School of Medicine&Chinese Center for Tropical Diseases Research,Shanghai 200000,China [4]Department of Respiratory and Critical Care Medicine,Ruijin Hospital,Shanghai Jiao Tong University School of Medicine,Shanghai 200000,China

出　　处：《Acta Biochimica et Biophysica Sinica》2022年第11期1740-1747,共8页生物化学与生物物理学报（英文版）

基　　金：This work was supported by the grants from the National Natural Science Foundation of China(Nos.81971896,81800190,and 81471908);the Natural Science Foundation of Shanghai Program(No.19ZR1428600);the National Innovative Research Team of High-Level Local Universities in Shanghai。

摘　　要：Pseudomonas aeruginosa is an opportunistic pathogen that causes chronic airway infection in bronchiectasis patients and is closely associated with poor prognosis.Strains isolated from chronically infected patients typically have a mucoid phenotype due to the overproduction of alginate.In this study,we isolate a P.aeruginosa strain from the sputum of a patient with bronchiectasis and find that a truncated mutation occurred in mucA,which is named mucA117.mucA117 causes the strain to transform into a mucoid phenotype,downregulates the expression of T3SS and inflammasome ligands such as fliC and allows it to avoid inflammasome activation.The truncated mutation of the MucA protein may help P.aeruginosa escape clearance by the immune system,enabling long-term colonization.

关 键 词：MucA BRONCHIECTASIS Type III secretion systems INFLAMMASOME 

分 类 号：R37[医药卫生—病原生物学]