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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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Related in: MedlinePlus

Intracellular NO and Ca2+ levels in the infected Caco-2 cells. Detection of NO and Ca2+ in Caco-2 cells, stained with DAF-FM DA and Fluo-3 AM, respectively and analyzed with flow cytometry (A) NO levels in uninfected cells and cells infected with RIMD, a pandemic strain (Vp024) or a non-pandemic strain (Vp029) at different time points. (B) NO levels in uninfected cells (control) and in cells infected with each strains at each specific time point. (C) Ca2+ levels in uninfected cells and cells infected with RIMD, a pandemic strain (Vp024), and a non-pandemic strain (Vp029) at different time points. (D) Ca2+ levels in uninfected cells (control) and in cells infected with each strain at each specific time point.
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Figure 5: Intracellular NO and Ca2+ levels in the infected Caco-2 cells. Detection of NO and Ca2+ in Caco-2 cells, stained with DAF-FM DA and Fluo-3 AM, respectively and analyzed with flow cytometry (A) NO levels in uninfected cells and cells infected with RIMD, a pandemic strain (Vp024) or a non-pandemic strain (Vp029) at different time points. (B) NO levels in uninfected cells (control) and in cells infected with each strains at each specific time point. (C) Ca2+ levels in uninfected cells and cells infected with RIMD, a pandemic strain (Vp024), and a non-pandemic strain (Vp029) at different time points. (D) Ca2+ levels in uninfected cells (control) and in cells infected with each strain at each specific time point.

Mentions: All strains clearly increased Ca2+ levels in the cells after infection. In contrast, cellular NO production decreased in the cells after infection by all the strains investigated (Figure 5). The intracellular pH of the cells infected with each strain was slightly lower than that of the control group and decreased slightly with the increase in time after infection. MMP of the infected cells increased, but then decreased 3 h after infection with each strain of Vibrio parahaemolyticus. This was clearly observed in the cells infected with Vp029 or Vp038, whereas MMP decreased only slightly in cells infected with Vp005 or Vp0024. However, MMP was stable in cells infected with RIMD (Table 4).


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)

Intracellular NO and Ca2+ levels in the infected Caco-2 cells. Detection of NO and Ca2+ in Caco-2 cells, stained with DAF-FM DA and Fluo-3 AM, respectively and analyzed with flow cytometry (A) NO levels in uninfected cells and cells infected with RIMD, a pandemic strain (Vp024) or a non-pandemic strain (Vp029) at different time points. (B) NO levels in uninfected cells (control) and in cells infected with each strains at each specific time point. (C) Ca2+ levels in uninfected cells and cells infected with RIMD, a pandemic strain (Vp024), and a non-pandemic strain (Vp029) at different time points. (D) Ca2+ levels in uninfected cells (control) and in cells infected with each strain at each specific time point.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 5: Intracellular NO and Ca2+ levels in the infected Caco-2 cells. Detection of NO and Ca2+ in Caco-2 cells, stained with DAF-FM DA and Fluo-3 AM, respectively and analyzed with flow cytometry (A) NO levels in uninfected cells and cells infected with RIMD, a pandemic strain (Vp024) or a non-pandemic strain (Vp029) at different time points. (B) NO levels in uninfected cells (control) and in cells infected with each strains at each specific time point. (C) Ca2+ levels in uninfected cells and cells infected with RIMD, a pandemic strain (Vp024), and a non-pandemic strain (Vp029) at different time points. (D) Ca2+ levels in uninfected cells (control) and in cells infected with each strain at each specific time point.
Mentions: All strains clearly increased Ca2+ levels in the cells after infection. In contrast, cellular NO production decreased in the cells after infection by all the strains investigated (Figure 5). The intracellular pH of the cells infected with each strain was slightly lower than that of the control group and decreased slightly with the increase in time after infection. MMP of the infected cells increased, but then decreased 3 h after infection with each strain of Vibrio parahaemolyticus. This was clearly observed in the cells infected with Vp029 or Vp038, whereas MMP decreased only slightly in cells infected with Vp005 or Vp0024. However, MMP was stable in cells infected with RIMD (Table 4).

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