Role of the sseK1 gene in the pathogenicity of Salmonella enterica serovar enteritidis in vitro and in vivo. (April 2018)

• Record Type: Journal Article
• Authors: Yang, Yadong; Yu, Chuan; Ding, Ke; Zhang, Chunjie; Liao, Chengshui; Jia, Yanyan; Li, Jing; Cheng, Xiangchao
• Is Part Of: Microbial pathogenesis. Volume 117(2018)
• Page Start: 270
• Page End: 275
• Publication Date: 2018-04
• Subjects: Salmonella enteritidis -- SseK1 -- Macrophages -- Biofilm formation -- Mouse; Pathogenic microorganisms -- Periodicals; Pathology, Molecular -- Periodicals; Communicable Diseases -- microbiology -- Periodicals; Communicable Diseases -- parasitology -- Periodicals; Micro-organismes pathogènes -- Périodiques; Pathologie moléculaire -- Périodiques; Electronic journals; 616.9041
• DOI: 10.1016/j.micpath.2018.02.030
• Languages: English
• ISSNs: 0882-4010

Abstract

Abstract: Salmonella enteritidis is a common food-borne pathogen associated with consumption of contaminated poultry meat and eggs, which frequently causes gastroenteritis in humans. Salmonella secreted effector K1 (SseK1), as a translocated and secreted protein has been identified to be essential for the virulence of Salmonella typhimurium in host cells. However, the role of the sseK1 gene in the pathogenicity of S. enteritidis remain unclear. In this study, a sseK1 deletion mutant of S. enteritidis was constructed and its biological characteristics were examined. It was found that the sseK1 deletion mutant did not affect the growth, adherence and invasion of Salmonella enteritidis when compared to the wild-type S. enteritidis. However, the mutant showed decreased formation of biofilm and significantly reduced intracellular survival of bacteria in activated mouse peritoneal macrophages, as well as showed reduced pathogenicity to a murine model by increasing the lethal dose 50% (LD50 ) value and decreasing the proliferation ratio of bacteria in vivo . Taken together, this study determined an important role for SseK1 in the pathogenicity of S. enteritidis in vitro and in vivo . Highlights: The deletion of sseK1 gene could decrease the biofilm formation of S. enteritidis. SseK1 was not associated with the ability of S. enteritidis to grow, adhere and invade. A sseK1 deletion mutant of S. enteritidis may reduce the proliferation of bacteria in mouse peritoneal macrophages. The deletion of sseK1 gene could increase the LD50 value and decrease the proliferation ratio of S. enteritidis in vivo.