Protective role of autophagy against
            <i>Vibrio cholerae</i>
            cytolysin, a pore-forming toxin from
            <i>V. cholerae</i>

Gutierrez, Maximiliano G.; Saka, Héctor Alex; Chinen, Isao; Zoppino, Felipe Carlos Martín; Yoshimori, Tamotsu; Bocco, José Luis; Colombo, María Isabel

doi:10.1073/pnas.0601437104

Cited by 161 publications

(160 citation statements)

References 49 publications

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“…Interestingly, recent studies indicate that the bacterial pore-forming toxins listeriolysin O and Vibrio cholerae's cytolysin trigger autophagy. 41,42 By analogy, the membrane channel activity of VacA within vacuoles may be sufficient to induce autophagy perhaps by inducing vacuolar damage as has recently been described for Salmonella. 43 Autophagy can also be triggered by the exposure of mammalian cells to stress conditions, such as nutrient deprivation.…”

Section: Discussionmentioning

confidence: 99%

Effect ofHelicobacter pylori’s vacuolating cytotoxin on the autophagy pathway in gastric epithelial cells

et al. 2009

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Section: Discussionmentioning

confidence: 99%

Effect ofHelicobacter pylori’s vacuolating cytotoxin on the autophagy pathway in gastric epithelial cells

et al. 2009

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“…A host cell can use autophagy to prevent the cytoplasmic replication or invasion of intracellular pathogens by engulfing the pathogens in autophagic vesicles and targeting them to lysosomes (28). In addition, recent work has shown that autophagy may provide defense against a secreted toxin from the noninvasive pathogen Vibrio cholerae (29). Alternatively, pathogens have evolved ways to usurp this pathway for their own benefit: for example, the intracellular pathogen Coxiella burnettii creates a replicative niche within autophagosomes where it can multiply and survive (30).…”

Section: Discussionmentioning

confidence: 99%

Vibrio parahaemolyticus orchestrates a multifaceted host cell infection by induction of autophagy, cell rounding, and then cell lysis

Burdette¹,

Yarbrough²,

Orvedahl

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

114

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The bacterial pathogen Vibrio parahaemolyticus utilizes a type III secretion system to cause death of host cells within hours of infection. We report that cell death is completely independent of apoptosis and occurs by a mechanism in which injection of multiple type III effectors causes induction of autophagy, cell rounding, and the subsequent release of cellular contents. Autophagy is detected by the appearance of lipidated light chain 3 (LC3) and by increases in punctae and vacuole formation. Electron microscopy reveals the production of early autophagic vesicles during infection. Consistent with phosphoinositide 3 (PI3) kinase playing a role in autophagy, treatment of infected cells with a PI3 kinase inhibitor attenuates autophagy in infected cells. Because many effectors are injected during a V. parahaemolyticus infection, it is not surprising that the presence of a sole PI3 kinase inhibitor does not prevent inevitable host-cell death. Our studies reveal an infection paradigm whereby an extracellular pathogen uses its type III secretion system to cause at least three parallel events that eventually result in the proinflammatory death of an infected host cell.host-pathogen ͉ type III secretion ͉ apoptosis ͉ effector ͉ inflammatory

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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: 99%

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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Protective role of autophagy against Vibrio cholerae cytolysin, a pore-forming toxin from V. cholerae

Cited by 161 publications

References 49 publications

Effect ofHelicobacter pylori’s vacuolating cytotoxin on the autophagy pathway in gastric epithelial cells

Effect ofHelicobacter pylori’s vacuolating cytotoxin on the autophagy pathway in gastric epithelial cells

Vibrio parahaemolyticus orchestrates a multifaceted host cell infection by induction of autophagy, cell rounding, and then cell lysis

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

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