Supplemental invasion of Salmonella from the perspective of Salmonella enterica serovars Kentucky and Typhimurium
Abstract Background Critical to the development of Salmonellosis in humans is the interaction of the bacterium with the epithelial lining of the gastrointestinal tract. Traditional scientific reasoning held type III secretion system (T3SS) as the virulence factor responsible for bacterial invasion....
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Language: | English |
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BMC
2017-04-01
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Series: | BMC Microbiology |
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Online Access: | http://link.springer.com/article/10.1186/s12866-017-0989-3 |
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author | Kevin Howe Sanaz Salehi R. Hartford Bailey John P. Brooks Robert Wills Mark L. Lawrence Attila Karsi |
author_facet | Kevin Howe Sanaz Salehi R. Hartford Bailey John P. Brooks Robert Wills Mark L. Lawrence Attila Karsi |
author_sort | Kevin Howe |
collection | DOAJ |
description | Abstract Background Critical to the development of Salmonellosis in humans is the interaction of the bacterium with the epithelial lining of the gastrointestinal tract. Traditional scientific reasoning held type III secretion system (T3SS) as the virulence factor responsible for bacterial invasion. In this study, field-isolated Salmonella enterica serovar Kentucky and a known human pathogen Salmonella enterica serovar Typhimurium were mutated and evaluated for the invasion of human colorectal adenocarcinoma epithelial cells. Results S. enterica serovar Kentucky was shown to actively invade a eukaryotic monolayer, though at a rate that was significantly lower than Typhimurium. Additionally, strains mutated for T3SS formation were less invasive than the wild-type strains, but the decrease in invasion was not significant in Kentucky. Conclusions Strains mutated for T3SS formation were able to initiate invasion of the eukaryotic monolayer to varying degrees based on strain, In the case of Kentucky, the mutated strain initiated invasion at a level that was not significantly different from the wild-type strain. A different result was observed for Typhimurium as the mutation significantly lowered the rate of invasion in comparison to the wild-type strain. |
first_indexed | 2024-12-22T11:17:16Z |
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id | doaj.art-f6e7a596a170473cb7628136d6a23598 |
institution | Directory Open Access Journal |
issn | 1471-2180 |
language | English |
last_indexed | 2024-12-22T11:17:16Z |
publishDate | 2017-04-01 |
publisher | BMC |
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series | BMC Microbiology |
spelling | doaj.art-f6e7a596a170473cb7628136d6a235982022-12-21T18:27:59ZengBMCBMC Microbiology1471-21802017-04-011711910.1186/s12866-017-0989-3Supplemental invasion of Salmonella from the perspective of Salmonella enterica serovars Kentucky and TyphimuriumKevin Howe0Sanaz Salehi1R. Hartford Bailey2John P. Brooks3Robert Wills4Mark L. Lawrence5Attila Karsi6Department of Pathobiology and Population Medicine, College of Veterinary Medicine, Mississippi State University, Mississippi StateDepartment of Pathobiology and Population Medicine, College of Veterinary Medicine, Mississippi State University, Mississippi StateDepartment of Pathobiology and Population Medicine, College of Veterinary Medicine, Mississippi State University, Mississippi StateUSDA-ARS, Genetics and Precision Agriculture UnitDepartment of Pathobiology and Population Medicine, College of Veterinary Medicine, Mississippi State University, Mississippi StateDepartment of Basic Sciences, College of Veterinary Medicine, Mississippi State UniversityDepartment of Basic Sciences, College of Veterinary Medicine, Mississippi State UniversityAbstract Background Critical to the development of Salmonellosis in humans is the interaction of the bacterium with the epithelial lining of the gastrointestinal tract. Traditional scientific reasoning held type III secretion system (T3SS) as the virulence factor responsible for bacterial invasion. In this study, field-isolated Salmonella enterica serovar Kentucky and a known human pathogen Salmonella enterica serovar Typhimurium were mutated and evaluated for the invasion of human colorectal adenocarcinoma epithelial cells. Results S. enterica serovar Kentucky was shown to actively invade a eukaryotic monolayer, though at a rate that was significantly lower than Typhimurium. Additionally, strains mutated for T3SS formation were less invasive than the wild-type strains, but the decrease in invasion was not significant in Kentucky. Conclusions Strains mutated for T3SS formation were able to initiate invasion of the eukaryotic monolayer to varying degrees based on strain, In the case of Kentucky, the mutated strain initiated invasion at a level that was not significantly different from the wild-type strain. A different result was observed for Typhimurium as the mutation significantly lowered the rate of invasion in comparison to the wild-type strain.http://link.springer.com/article/10.1186/s12866-017-0989-3SalmonellaKentuckyTyphimuriumType III Secretion SystemInvasionInternalization |
spellingShingle | Kevin Howe Sanaz Salehi R. Hartford Bailey John P. Brooks Robert Wills Mark L. Lawrence Attila Karsi Supplemental invasion of Salmonella from the perspective of Salmonella enterica serovars Kentucky and Typhimurium BMC Microbiology Salmonella Kentucky Typhimurium Type III Secretion System Invasion Internalization |
title | Supplemental invasion of Salmonella from the perspective of Salmonella enterica serovars Kentucky and Typhimurium |
title_full | Supplemental invasion of Salmonella from the perspective of Salmonella enterica serovars Kentucky and Typhimurium |
title_fullStr | Supplemental invasion of Salmonella from the perspective of Salmonella enterica serovars Kentucky and Typhimurium |
title_full_unstemmed | Supplemental invasion of Salmonella from the perspective of Salmonella enterica serovars Kentucky and Typhimurium |
title_short | Supplemental invasion of Salmonella from the perspective of Salmonella enterica serovars Kentucky and Typhimurium |
title_sort | supplemental invasion of salmonella from the perspective of salmonella enterica serovars kentucky and typhimurium |
topic | Salmonella Kentucky Typhimurium Type III Secretion System Invasion Internalization |
url | http://link.springer.com/article/10.1186/s12866-017-0989-3 |
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