<i>Vibrio parahaemolyticus</i>thermostable direct hemolysin can induce an apoptotic cell death in Rat-1 cells from inside and ouside of the cells

Naim, Rochman; Yanagihara, Itaru; Iida, Tetsuya; Honda, Takeshi

doi:10.1111/j.1574-6968.2001.tb10527.x

Cited by 46 publications

(15 citation statements)

References 28 publications

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“…The same experiments have been repeated in case of HT-29, another colon carcinoma cell line and the results obtained are similar like that of COLO-205 (data not shown). In contrast to the observation made by Naim et al , 2001 [43] in rat-1 cells, our results suggest that apoptosis and cytotoxicity are not contributing to the reduction of proliferation rate in colon carcinoma cells and this reduction appears to be caused by decrease in cell proliferation.…”

Section: Discussioncontrasting

confidence: 99%

Thermostable Direct Hemolysin Downregulates Human Colon Carcinoma Cell Proliferation with the Involvement of E-Cadherin, and β-Catenin/Tcf-4 Signaling

et al. 2011

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BackgroundColon cancers are the frequent causes of cancer mortality worldwide. Recently bacterial toxins have received marked attention as promising approaches in the treatment of colon cancer. Thermostable direct hemolysin (TDH) secreted by Vibrio parahaemolyticus causes influx of extracellular calcium with the subsequent rise in intracellular calcium level in intestinal epithelial cells and it is known that calcium has antiproliferative activity against colon cancer.Key ResultsIn the present study it has been shown that TDH, a well-known traditional virulent factor inhibits proliferation of human colon carcinoma cells through the involvement of CaSR in its mechanism. TDH treatment does not induce DNA fragmentation, nor causes the release of lactate dehydrogenase. Therefore, apoptosis and cytotoxicity are not contributing to the TDH-mediated reduction of proliferation rate, and hence the reduction appears to be caused by decrease in cell proliferation. The elevation of E-cadherin, a cell adhesion molecule and suppression of β-catenin, a proto-oncogene have been observed in presence of CaSR agonists whereas reverse effect has been seen in presence of CaSR antagonist as well as si-RNA in TDH treated cells. TDH also triggers a significant reduction of Cyclin-D and cdk2, two important cell cycle regulatory proteins along with an up regulation of cell cycle inhibitory protein p27Kip1 in presence of CaSR agonists.ConclusionTherefore TDH can downregulate colonic carcinoma cell proliferation and involves CaSR in its mechanism of action. The downregulation occurs mainly through the involvement of E-cadherin-β-catenin mediated pathway and the inhibition of cell cycle regulators as well as upregulation of cell cycle inhibitors.

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Section: Discussioncontrasting

confidence: 99%

Thermostable Direct Hemolysin Downregulates Human Colon Carcinoma Cell Proliferation with the Involvement of E-Cadherin, and β-Catenin/Tcf-4 Signaling

et al. 2011

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“…To analyze the tissue distribution of TcMyD88, the following tissues were collected from six healthy adult T. crocea: siphonal mantle, pedal mantle, inner mantle, byssus gland, pedis, heart, gill and hemocytes. For analysis of the developmental expression patterns of TcMyD88, samples of 0, 0.5, 1,4,12,16,24,48,72,96, and 120 h-developing embryos were also obtained.…”

Section: Animals Tissue Embryonic Development Collection and Challementioning

confidence: 99%

Mechanistic molecular responses of the giant clam Tridacna crocea to Vibrio coralliilyticus challenge

Zhao

Zhou

et al. 2020

PLoS ONE

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Vibrio coralliilyticus is a pathogen of coral and mollusk, contributing to dramatic losses worldwide. In our study, we found that V. coralliilyticus challenge could directly affect adult Tridacna crocea survival; there were dead individuals appearing at 6 h post infection, and there were 45.56% and 56.78% mortality rates in challenged groups after 36 h of infection. The apoptosis rate of hemocytes was significantly increased by 1.8-fold at 6 h after V. coralliilyticus injection. To shed light on the mechanistic molecular responses of T. crocea to V. coralliilyticus infection, we used transcriptome sequencing analysis and other relevant techniques to analyze T. crocea hemocytes at 0 h, 6 h, 12 h and 24 h after V. coralliilyticus challenge. Our results revealed that the total numbers of unigenes and DEGs were 195651 and 3446, respectively. Additional details were found by KEGG pathway enrichment analysis, where DEGs were significantly enriched in immune-related signaling pathways, such as the TLR signaling pathway, and some were associated with signaling related to apoptosis. Quantitative validation results illustrated that with exposure to V. coralliilyticus, the expression of TLR pathway members, TLR, MyD88, IRAK4, TRAF6, and IкB-α, were significantly upregulated (by 22.9-, 9.6-, 4.0-, 3.6-, and 3.9-fold, respectively) at 6 h. The cytokine-related gene IL-17 exhibited an increase of 6.3-fold and 10.5-fold at 3 h and 6 h, respectively. The apoptosis-related gene IAP1 was dramatically increased by 2.99-fold at 6 h. These results indicate that adult T. crocea could initiate the TLR pathway to resist V. coralliilyticus, which promotes the release of inflammatory factors such as IL-17 and leads to the activation of a series of outcomes, such as apoptosis. The response mechanism is related to the T. crocea immunoreaction stimulated by V. coralliilyticus, providing a theoretical basis for understanding T. crocea immune response mechanisms.

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“…This hemolysis is called the Kanagawa phenomenon (KP), which has been considered to be a useful marker to distinguish pathogenic from non-pathogenic strains [6], [7]. Thermostable direct hemolysin (TDH) is responsible for KP and purified TDH shows a number of biological effects, such as erythrocyte lysis, cytotoxicity and induction of fluid accumulation in an ileal loop model [6], [8], [9], [10], [11], [12], [13], [14], [15], [16], [17]. Thus, TDH has been considered a major virulence factor of V. parahaemolyticus .…”

Section: Introductionmentioning

confidence: 99%

Two Regulators of Vibrio parahaemolyticus Play Important Roles in Enterotoxicity by Controlling the Expression of Genes in the Vp-PAI Region

et al. 2010

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Vibrio parahaemolyticus is an important pathogen causing food-borne disease worldwide. An 80-kb pathogenicity island (Vp-PAI), which contains two tdh (thermostable direct hemolysin) genes and a set of genes for the type III secretion system (T3SS2), is closely related to the pathogenicity of this bacterium. However, the regulatory mechanisms of Vp-PAI's gene expression are poorly understood. Here we report that two novel ToxR-like transcriptional regulatory proteins (VtrA and VtrB) regulate the expression of the genes encoded within the Vp-PAI region, including those for TDH and T3SS2-related proteins. Expression of vtrB was under control of the VtrA, as vector-expressed vtrB was able to recover a functional protein secretory capacity for T3SS2, independent of VtrA. Moreover, these regulatory proteins were essential for T3SS2-dependent biological activities, such as in vitro cytotoxicity and in vivo enterotoxicity. Enterotoxic activities of vtrA and/or vtrB deletion strains derived from the wild-type strain were almost absent, showing fluid accumulation similar to non-infected control. Whole genome transcriptional profiling of vtrA or vtrB deletion strains revealed that the expression levels of over 60 genes were downregulated significantly in these deletion mutant strains and that such genes were almost exclusively located in the Vp-PAI region. These results strongly suggest that VtrA and VtrB are master regulators for virulence gene expression in the Vp-PAI and play critical roles in the pathogenicity of this bacterium.

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Vibrio parahaemolyticusthermostable direct hemolysin can induce an apoptotic cell death in Rat-1 cells from inside and ouside of the cells

Cited by 46 publications

References 28 publications

Thermostable Direct Hemolysin Downregulates Human Colon Carcinoma Cell Proliferation with the Involvement of E-Cadherin, and β-Catenin/Tcf-4 Signaling

Thermostable Direct Hemolysin Downregulates Human Colon Carcinoma Cell Proliferation with the Involvement of E-Cadherin, and β-Catenin/Tcf-4 Signaling

Mechanistic molecular responses of the giant clam Tridacna crocea to Vibrio coralliilyticus challenge

Two Regulators of Vibrio parahaemolyticus Play Important Roles in Enterotoxicity by Controlling the Expression of Genes in the Vp-PAI Region

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