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The role of SEF14 fimbriae in virulence remains to be elucidated and in this study, we showed that sefA mutant constructed in the wild-type (WT) Salmonella enteritidis strain 50336 displayed increased invasion to IPEC-J2 cell lines and survival in mouse peritoneal macrophages, and the lethal dose 50% (LD50) in 6-week-old Balb/c mice intra-peritoneally injected with WT S. enteritidis strain decreased significantly upon deletion of sefA indicating their role in virulence. Overall, these results demonstrated that expression of sefA of SEF14 fimbriae enhances S. enteritidis adhesion to epithelial cells and survival in macrophages and contributes to S. enteritidis virulence in mice.
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http://dx.doi.org/10.1016/j.micpath.2013.07.002 | DOI Listing |
Microb Pathog
January 2019
College of Veterinary Medicine (Institute of Comparative Medicine), Yangzhou University, Yangzhou 225009, China; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou 225009, China. Electronic address:
Infection with Salmonella Enteritidis (SE) is one of the main causes for food- and water-borne diseases, and is a major concern to public health for both humans and animals worldwide. Some fimbrial antigens expressed by SE strains have been described and characterized, containing SEF14, SEF17, SEF21, long polar fimbriae and plasmid-encoded fimbriae, they play a role in bacterial survival in the host or external environment. However, their functions remain to be well elucidated, with the initial attachment and binding for fimbriae-mediated SE infections only minimally understood.
View Article and Find Full Text PDFAvian Dis
September 2013
Institute of Immunology, College of Life Science and Technology, Dalian University, 10-Xuefu Avenue, Dalian Economical and Technological Development Zone, Liaoning 116622, China.
In order to generate Salmonella enterica serovar Enteritidis (Salmonella Enteritidis) fimbriae, SEF14, the sefA gene, which encodes the main subunit of the SEF14 fimbrial protein, was amplified from Salmonella Enteritidis by polymerase chain reaction (PCR) and subcloned into a prokaryotic expression vector pET-28a(+) to yield pET-28a(+)-sefA. The recombinant SefA (rSefA) protein was highly expressed and purified by nickel-affinity chromatography. Liposome-associated rSefA was prepared for oral immunization to seek protective efficacy for intestinal infection with Salmonella Enteritidis.
View Article and Find Full Text PDFMicrob Pathog
November 2013
Jiangsu Institute of Poultry Science, Yangzhou 225125, China; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou 225009, China.
The role of SEF14 fimbriae in virulence remains to be elucidated and in this study, we showed that sefA mutant constructed in the wild-type (WT) Salmonella enteritidis strain 50336 displayed increased invasion to IPEC-J2 cell lines and survival in mouse peritoneal macrophages, and the lethal dose 50% (LD50) in 6-week-old Balb/c mice intra-peritoneally injected with WT S. enteritidis strain decreased significantly upon deletion of sefA indicating their role in virulence. Overall, these results demonstrated that expression of sefA of SEF14 fimbriae enhances S.
View Article and Find Full Text PDFInfect Immun
April 2013
Department of Microbiology and Immunology, The University of Melbourne, Victoria, Australia.
AraC-like regulators play a key role in the expression of virulence factors in enteric pathogens, such as enteropathogenic Escherichia coli (EPEC), enterotoxigenic E. coli, enteroaggregative E. coli, and Citrobacter rodentium.
View Article and Find Full Text PDFAppl Environ Microbiol
September 2012
U.S. Department of Agriculture, Agricultural Research Service, Athens, Georgia, USA.
Salmonella enterica serovar Enteritidis is one of a few Salmonella enterica serotypes that has SEF14 fimbriae encoded by the sef operon, which consists of 4 cotranscribed genes, sefABCD, regulated by sefR. A parental strain was used to construct a sefD mutant and its complement, and all 3 strains were compared for gene expression, metabolic properties, and virulence characteristics in hens. Transcription of sefD by wild type was suppressed at 42°C and absent for the mutant under conditions where the complemented mutant had 10(3) times higher transcription.
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