roles of putative type ii secretion and type iv pilus systems in the virulence of uropathogenic escherichia coli假定的ii型分泌的角色和iv型纤毛系统uropathogenic大肠杆菌的毒力.pdfVIP

roles of putative type ii secretion and type iv pilus systems in the virulence of uropathogenic escherichia coli假定的ii型分泌的角色和iv型纤毛系统uropathogenic大肠杆菌的毒力.pdf

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roles of putative type ii secretion and type iv pilus systems in the virulence of uropathogenic escherichia coli假定的ii型分泌的角色和iv型纤毛系统uropathogenic大肠杆菌的毒力

Roles of Putative Type II Secretion and Type IV Pilus Systems in the Virulence of Uropathogenic Escherichia coli 1¤ 2 2 1 2 Ritwij Kulkarni , Bijaya K. Dhakal , E. Susan Slechta , Zachary Kurtz , Matthew A. Mulvey , David G. Thanassi1* 1 Center for Infectious Diseases, Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, New York, United States of America, 2 Department of Pathology, Division of Cell Biology and Immunology, University of Utah, Salt Lake City, Utah, United States of America Abstract Background: Type II secretion systems (T2SS) and the evolutionarily related type IV pili (T4P) are important virulence determinants in many Gram-negative bacterial pathogens. However, the roles of T2SS and T4P in the virulence of extraintestinal pathogenic Escherichia coli have not been determined. Methodology/Principal Findings: To investigate the functions of putative T2SS and T4P gene clusters present in the model uropathogenic E. coli (UPEC) strains UTI89 and CFT073, we deleted the secretin gene present in each cluster. The secretin forms a channel in the outer membrane that is essential for the function of T2S and T4P systems. We compared the secretin deletion mutants with their wild type counterparts using tissue culture assays and the CBA/J mouse model of ascending urinary tract infection. No deficiencies were observed with any of the mutants in adherence, invasion or replication in human bladder or kidney cell lines, but UTI89 DhofQ and UTI89 DgspD exhibited approximately 2-fold defects in fluxing out of bladder epithelial cells. In the mouse infection model, each of the knockout mutants was able to establish successful

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