Within-macrophages replication dynamics of Klebsiella pneumoniae
发布时间 :2019-10-17  阅读次数 :6273

报 告 人:Professor Marco R. Oggioni

Dept of Genetics and Genome Biology,

University of Leicester, Leicester, UK

报告时间:2019年10月22日(星期二) 13:00-14:00

报告地点:徐汇校区哲生馆一楼会议室

联 系 人:欧竑宇

 

报告人简介:

MRO has two main areas of research interest which are the discovery of specific details in the interaction of pathogenic bacteria with the host that could lead to new treatment options and the analysis of antimicrobial resistance determinants. MRO addresses the study of bacterial virulence mechanisms, by use of genomic tools, the exploration of microbial physiology, and the detailed analysis of events occurring in experimental infection models. Main scope of this work is the recognition of specific phases characterising microbial physiology during infection with the aim of identification of novel drug targets.

 

Since 2013 MRO joined the Department of Genetics and Genome Biology of the University of Leicester as a Chair in Microbial Genetics and, since 2015, MRO has in addition an Honorary Microbiology Consultant Contract with the University of Leicester Hospitals NHS Trust. He is co-chair of the Leicester Microbial Sciences and Infectious Disease LeMID Network.

 

报告摘要:

Klebsiella pneumoniae (Kp) is a Gram-negative human pathogen. Hypervirulent lineages hvKp (predominantly capsule type K1/K2) are unique in their clinical presentation as they cause bacteraemic hepatic and splenic abscesses, occurring also in immunocompetent subjects. In addition, K2 ST25 strains are responsible for invasive disease in pigs. We have recently shown that intracellular replication of Streptococcus pneumoniae precedes the onset of bacteraemia. We aimed to test the hypothesis that hvKp abscess formation starts after within macrophage replication.Our data indicate that the efficient replication of hvKp isolates within CD169+ macrophages is the most likely mechanism for the origin of K. pneumoniae hepatic and splenic abscesses which characterise human disease.