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Vibrio parahaemolyticus strengthens their virulence through modulation of cellular reactive oxygen species in vitro.

El-Malah SS, Yang Z, Hu M, Li Q, Pan Z, Jiao X - Front Cell Infect Microbiol (2014)

Bottom Line: Our results show that Vp adheres to cell monolayers and can invade non-phagocytic cells.It also survives and persists in non-phagocytic cells by modulating reactive oxygen species (ROS), allowing its replication, and resulting in complete cellular destruction.We conclude that the pathogenicity of Vp is based on its capacities for adhesion and invasion.

View Article: PubMed Central - PubMed

Affiliation: Jiangsu Key Laboratory of Zoonosis/Jiangsu Co-Innovation Center for the Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University Yangzhou, China.

ABSTRACT
Vibrio parahaemolyticus (Vp) is one of the emergent food-borne pathogens that are commensally associated with various shellfish species throughout the world. It is strictly environmental and many strains are pathogenic to humans. The virulent strains cause distinct diseases, including wound infections, septicemia, and most commonly, acute gastroenteritis, which is acquired through the consumption of raw or undercooked seafood, especially shellfish. Vp has two type three secretion systems (T3SSs), which triggering its cytotoxicity and enterotoxicity via their effectors. To better understand the pathogenesis of Vp, we established a cell infection model in vitro using a non-phagocytic cell line. Caco-2 cells were infected with different strains of Vp (pandemic and non-pandemic strains) and several parameters of cytotoxicity were measured together with adhesion and invasion indices, which reflect the pathogen's virulence. Our results show that Vp adheres to cell monolayers and can invade non-phagocytic cells. It also survives and persists in non-phagocytic cells by modulating reactive oxygen species (ROS), allowing its replication, and resulting in complete cellular destruction. We conclude that the pathogenicity of Vp is based on its capacities for adhesion and invasion. Surprisingly's; enhanced of ROS resistance period could promote the survival of Vp inside the intestinal tract, facilitating tissue infection by repressing the host's oxidative stress response.

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Invasion index of Vibrio parahaemolyticus in Caco-2 cells. Caco-2 cells were infected with Vibrio parahaemolyticus strains. The reported values are the means ± SEM of three independent experiments (n = 6). (A) Uninfected Caco-2 cells were used as the control. (B–E) Caco-2 cells infected with RIMD [MOI] = 100:1 at 30, 60, 120, and 180 min, respectively (100X, oil immersion). (F) Means invasion indices differed statistically significantly from one another on Two-Way ANOVA (**P < 0.01; ***P < 0.001).
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Figure 2: Invasion index of Vibrio parahaemolyticus in Caco-2 cells. Caco-2 cells were infected with Vibrio parahaemolyticus strains. The reported values are the means ± SEM of three independent experiments (n = 6). (A) Uninfected Caco-2 cells were used as the control. (B–E) Caco-2 cells infected with RIMD [MOI] = 100:1 at 30, 60, 120, and 180 min, respectively (100X, oil immersion). (F) Means invasion indices differed statistically significantly from one another on Two-Way ANOVA (**P < 0.01; ***P < 0.001).

Mentions: No bacteria were recovered from the RIMD-treated cells at 30, 60, or 120 min after infection, but bacteria were recovered at 180 min (Figures 2A–E). The same observation was made of all cells infected with Vp005, Vp029, or Vp038 after 30 min, but no bacteria were recovered from Vp029-treated cells at 60 min. There were no significant differences between any of the strains after 180 min, but the significant differences were observed between RIMD and Vp024 at two time points (60 and 120 min) and between RIMD and Vp029, and between RIMD and Vp038 at 120 min. There were also significant differences between Vp005 and Vp024, Vp005 and Vp029, and Vp005 and Vp038 at the same time (120 min), and a significant difference between Vp024 and Vp029 at 60 min after infection (Figure 2F) and (Table 3).


Vibrio parahaemolyticus strengthens their virulence through modulation of cellular reactive oxygen species in vitro.

El-Malah SS, Yang Z, Hu M, Li Q, Pan Z, Jiao X - Front Cell Infect Microbiol (2014)

Invasion index of Vibrio parahaemolyticus in Caco-2 cells. Caco-2 cells were infected with Vibrio parahaemolyticus strains. The reported values are the means ± SEM of three independent experiments (n = 6). (A) Uninfected Caco-2 cells were used as the control. (B–E) Caco-2 cells infected with RIMD [MOI] = 100:1 at 30, 60, 120, and 180 min, respectively (100X, oil immersion). (F) Means invasion indices differed statistically significantly from one another on Two-Way ANOVA (**P < 0.01; ***P < 0.001).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4269196&req=5

Figure 2: Invasion index of Vibrio parahaemolyticus in Caco-2 cells. Caco-2 cells were infected with Vibrio parahaemolyticus strains. The reported values are the means ± SEM of three independent experiments (n = 6). (A) Uninfected Caco-2 cells were used as the control. (B–E) Caco-2 cells infected with RIMD [MOI] = 100:1 at 30, 60, 120, and 180 min, respectively (100X, oil immersion). (F) Means invasion indices differed statistically significantly from one another on Two-Way ANOVA (**P < 0.01; ***P < 0.001).
Mentions: No bacteria were recovered from the RIMD-treated cells at 30, 60, or 120 min after infection, but bacteria were recovered at 180 min (Figures 2A–E). The same observation was made of all cells infected with Vp005, Vp029, or Vp038 after 30 min, but no bacteria were recovered from Vp029-treated cells at 60 min. There were no significant differences between any of the strains after 180 min, but the significant differences were observed between RIMD and Vp024 at two time points (60 and 120 min) and between RIMD and Vp029, and between RIMD and Vp038 at 120 min. There were also significant differences between Vp005 and Vp024, Vp005 and Vp029, and Vp005 and Vp038 at the same time (120 min), and a significant difference between Vp024 and Vp029 at 60 min after infection (Figure 2F) and (Table 3).

Bottom Line: Our results show that Vp adheres to cell monolayers and can invade non-phagocytic cells.It also survives and persists in non-phagocytic cells by modulating reactive oxygen species (ROS), allowing its replication, and resulting in complete cellular destruction.We conclude that the pathogenicity of Vp is based on its capacities for adhesion and invasion.

View Article: PubMed Central - PubMed

Affiliation: Jiangsu Key Laboratory of Zoonosis/Jiangsu Co-Innovation Center for the Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University Yangzhou, China.

ABSTRACT
Vibrio parahaemolyticus (Vp) is one of the emergent food-borne pathogens that are commensally associated with various shellfish species throughout the world. It is strictly environmental and many strains are pathogenic to humans. The virulent strains cause distinct diseases, including wound infections, septicemia, and most commonly, acute gastroenteritis, which is acquired through the consumption of raw or undercooked seafood, especially shellfish. Vp has two type three secretion systems (T3SSs), which triggering its cytotoxicity and enterotoxicity via their effectors. To better understand the pathogenesis of Vp, we established a cell infection model in vitro using a non-phagocytic cell line. Caco-2 cells were infected with different strains of Vp (pandemic and non-pandemic strains) and several parameters of cytotoxicity were measured together with adhesion and invasion indices, which reflect the pathogen's virulence. Our results show that Vp adheres to cell monolayers and can invade non-phagocytic cells. It also survives and persists in non-phagocytic cells by modulating reactive oxygen species (ROS), allowing its replication, and resulting in complete cellular destruction. We conclude that the pathogenicity of Vp is based on its capacities for adhesion and invasion. Surprisingly's; enhanced of ROS resistance period could promote the survival of Vp inside the intestinal tract, facilitating tissue infection by repressing the host's oxidative stress response.

Show MeSH
Related in: MedlinePlus