Vibrio cholerae cytolysin is essential for high enterotoxicity and apoptosis induction produced by a cholera toxin gene-negative V. cholerae non-O1, non-O139 strain

Saka, Héctor Alex; Bidinost, Carla; Sola, Claudia; Carranza, Pablo; Collino, César; Ortiz, Susana; Echenique, José; Bocco, José Luis

doi:10.1016/j.micpath.2007.08.013

Cited by 52 publications

(67 citation statements)

References 62 publications

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“…In this context, it has been reported that tumor promoter agents (e.g., phorbol esters), growth factors, and DNA damage are involved in the regulation of KLF6 protein level correlating with the proliferation control and cell death (22,26,36). Moreover, recent results indicate that the endogenous KLF6 protein level is responsive to the intoxication triggered by the Vibrio cholerae cytolysin (Saka H. A., Andreoli V., and Bocco J. L., unpublished), which is able to trigger apoptosis and autophagy in human intestinal epithelial cells (50)(51)(52).…”

Section: Klf6mentioning

confidence: 98%

Biology of Krüppel‐like factor 6 transcriptional regulator in cell life and death

2010

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SummaryAn essential role for the Krü ppel-like transcription factor family has been determined in the regulation of remarkable processes including cell proliferation, differentiation, signal transduction, oncogenesis, and cell death. A member of this group, Krü ppel-like factor 6 (KLF6), identified on the basis of its ability to regulate a group of genes belonging to the carcinoembryonic antigen gene family, has been involved in human carcinogenesis. Early studies proposed a tumor suppressor function for KLF6 because of its ability to reduce cell proliferation through several biochemical mechanisms including regulation of cell cycle components, oncogene products, and apoptosis. Mutations within the klf6 gene, decreased expression and/or loss-of-heterozygosity were associated with the development of different human malignancies, and, hence, further supporting the tumor suppressor function of KLF6. This view has been challenged by other studies in distinct types of human cancers describing infrequent genetic alterations of klf6 gene or even enhanced expression in some tumors. The scenario about KLF6 function became still more complex as the description of oncogenic KLF6 splice variant 1 (SV1) with dominant negative activity against the wild type KLF6 (wtKLF6) protein. Additionally, increased evidence is suggesting that KLF6 is a bonafide target of several signaling cascades, which ultimate regulatory effect on this protein could drive decisions of cell life and death, facing the dilemma about how wtKLF6 could be involved in both processes. These apparently conflicting situations, emerged by apparently opposite effects mediated by wtKLF6, may be related, at least in part, to the biological cross-talk with the c-Jun oncoprotein. Depending on the stimulus received by the cell, wtKLF6 interaction with c-Jun determines different cell outcomes such as proliferation control or apoptosis. Thus, KLF6 responsiveness represents a kind of cell warning signal on receiving different stimuli, including oncogenic activation and microbial infections, orchestrating the implementation of proliferation and apoptotic programs.

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Section: Klf6mentioning

confidence: 98%

Biology of Krüppel‐like factor 6 transcriptional regulator in cell life and death

2010

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“…In rabbit ex vivo ileal loops, V. cholerae VCC induces recruitment of PMNs, vascular alterations (edema and dilation of lymph vessels), necrosis and apoptosis of the epithelium, and congestion of the mucosa, all likely contributing to barrier dysfunction (205). Non-O1 and non-O139 serotype V. cholerae strains, which are usually cholera toxin (CT) and toxin-coregulated pilus A (TcpA) negative, can still cause watery diarrhea (205,206).…”

Section: Pft-induced Barrier Dysfunctionmentioning

confidence: 99%

Role of Pore-Forming Toxins in Bacterial Infectious Diseases

Los

Randis

Aroian

et al. 2013

Microbiol Mol Biol Rev

350

351

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SUMMARY Pore-forming toxins (PFTs) are the most common bacterial cytotoxic proteins and are required for virulence in a large number of important pathogens, including Streptococcus pneumoniae , group A and B streptococci, Staphylococcus aureus , Escherichia coli , and Mycobacterium tuberculosis . PFTs generally disrupt host cell membranes, but they can have additional effects independent of pore formation. Substantial effort has been devoted to understanding the molecular mechanisms underlying the functions of certain model PFTs. Likewise, specific host pathways mediating survival and immune responses in the face of toxin-mediated cellular damage have been delineated. However, less is known about the overall functions of PFTs during infection in vivo . This review focuses on common themes in the area of PFT biology, with an emphasis on studies addressing the roles of PFTs in in vivo and ex vivo models of colonization or infection. Common functions of PFTs include disruption of epithelial barrier function and evasion of host immune responses, which contribute to bacterial growth and spreading. The widespread nature of PFTs make this group of toxins an attractive target for the development of new virulence-targeted therapies that may have broad activity against human pathogens.

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“…Thus, the chloride secretion characteristic of STb-induced diarrhea could play a role in the activation of caspases observed in the current study. Cytolysin of Vibrio cholerae, like enterotoxin, possesses the capacity of inducing apoptosis and histological damages during diarrhea [46]. Furthermore, the inhibition of the apoptosis mediated by toxin A of Clostridium difficile resulted in reduced fluid accumulation and mucosal disruption of rabbit intestinal loops [23] providing additional evidence of diarrhea and apoptosis relationship.…”

Section: Discussionmentioning

confidence: 99%

Escherichia coli STb toxin induces apoptosis in intestinal epithelial cell lines

Syed

Dubreuil

2012

Microbial Pathogenesis

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Vibrio cholerae cytolysin is essential for high enterotoxicity and apoptosis induction produced by a cholera toxin gene-negative V. cholerae non-O1, non-O139 strain

Cited by 52 publications

References 62 publications

Biology of Krüppel‐like factor 6 transcriptional regulator in cell life and death

Biology of Krüppel‐like factor 6 transcriptional regulator in cell life and death

Role of Pore-Forming Toxins in Bacterial Infectious Diseases

Escherichia coli STb toxin induces apoptosis in intestinal epithelial cell lines

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