the salmonella spi2 effector ssei mediates long-term systemic infection by modulating host cell migration沙门氏菌spi2效应ssei介导长期系统性感染通过调节宿主细胞迁移.pdfVIP

The Salmonella SPI2 Effector SseI Mediates Long-Term Systemic Infection by Modulating Host Cell Migration 1. 1. 1 1 1 Laura M. McLaughlin , Gregory R. Govoni , Christiane Gerke , Smita Gopinath , Kaitian Peng , Grace 1 1 2 2 2 2 Laidlaw , Yueh-Hsiu Chien , Ha-Won Jeong , Zhigang Li , Matthew D. Brown , David B. Sacks , Denise Monack1* 1 Department of Microbiology and Immunology, Stanford University Medical Center, Stanford, California, United States of America, 2 Department of Pathology, Harvard Medical School, Brigham and Women’s Hospital, Boston, Massachusetts, United States of America Abstract Host-adapted strains of Salmonella enterica cause systemic infections and have the ability to persist systemically for long periods of time despite the presence of a robust immune response. Chronically infected hosts are asymptomatic and ¨ transmit disease to naıve hosts via fecal shedding of bacteria, thereby serving as a critical reservoir for disease. We show that the bacterial effector protein SseI (also called SrfH), which is translocated into host cells by the Salmonella Pathogenicity Island 2 (SPI2) type III secretion system (T3SS), is required for Salmonella typhimurium to maintain a long-term chronic systemic infection in mice. SseI inhibits normal cell migration of primary macrophages and dendritic cells (DC) in vitro, and such inhibition requires the host factor IQ motif containing GTPase activating protein 1 (IQGAP1), an important re