Helicobacter pylori VacA Induces Programmed Necrosis in Gastric Epithelial Cells

Radin, Jana N.; González-Rivera, Christian; Ivie, Susan E.; McClain, Mark S.; Cover, Timothy L.

doi:10.1128/iai.01370-10

Cited by 100 publications

(80 citation statements)

References 78 publications

(136 reference statements)

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“…The pore and channel forming by the N-terminal p33 domain alone drives pleiotropic cellular activities of VacA; i.e. vacuolation, mitochondria damage, apoptosis (10,47), autophagy (28,29), and programmed necrosis (27), suggesting that VacA may be characterized as a pore-forming toxin (47). Another study has indicated that both p33 and p55 are required to form a functional channel in the inner mitochondria membrane and trigger apoptosis (49).…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, VacA-induced cell death may occur through a programmed necrosis pathway in a caspase-independent process in AZ-521 cells (27). Therefore, we examined whether VacA-induced cell death resulted from autophagy via an LRP1-dependent pathway.…”

Section: Lrp-1 But Not Rptps Mediates Cleavage Of Caspase-7 and Parmentioning

confidence: 99%

“…Over the last 10 years, studies have focused on the mechanism of cell death resulting from mitochondrial damage caused by VacA (10,12,13,27). Additional recent studies have shown that VacA induces autophagy, but the pathway has not been identified (28,29).…”

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confidence: 99%

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Low-density Lipoprotein Receptor-related Protein-1 (LRP1) Mediates Autophagy and Apoptosis Caused by Helicobacter pylori VacA

Yahiro

Satoh

Nakano

et al. 2012

Journal of Biological Chemistry

127

117

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Section: Discussionmentioning

confidence: 99%

Section: Lrp-1 But Not Rptps Mediates Cleavage Of Caspase-7 and Parmentioning

confidence: 99%

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Low-density Lipoprotein Receptor-related Protein-1 (LRP1) Mediates Autophagy and Apoptosis Caused by Helicobacter pylori VacA

Yahiro

Satoh

Nakano

et al. 2012

Journal of Biological Chemistry

127

117

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“…A current model proposes that VacA monomers interact with the plasma membrane and subsequently oligomerize, which allows the formation of VacA pores in cell membranes (9). VacA causes a wide range of alterations in human gastric cells (9), including the formation of large cytoplasmic vacuoles (11,40), permeabilization of the plasma membrane (65), reduction of mitochondrial transmembrane potential (19,24,26,74), mitochondrial cytochrome c release (19,24,26,74), mitochondrial fragmentation (35), activation of mitogen-activated protein kinases (49), induction of autophagy (67), and cell death (13,26,35,53). Most of these effects (but not all) are dependent on membrane channel formation by VacA (30,34,46,71).…”

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confidence: 99%

The Intermediate Region of Helicobacter pylori VacA Is a Determinant of Toxin Potency in a Jurkat T Cell Assay

et al. 2012

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ABSTRACTColonization of the human stomach withHelicobacter pyloriis a risk factor for peptic ulceration, noncardia gastric adenocarcinoma, and gastric lymphoma. The secreted VacA toxin is an importantH. pylorivirulence factor that causes multiple alterations in gastric epithelial cells and T cells. Several families ofvacAalleles have been described, andH. pyloristrains containing certainvacAtypes (s1, i1, and m1) are associated with an increased risk of gastric disease, compared to strains containing othervacAtypes (s2, i2, and m2). Thus far, there has been relatively little study of the role of the VacA intermediate region (i-region) in toxin activity. In this study, we compared the ability of i1 and i2 forms of VacA to cause functional alterations in Jurkat cells. To do this, we manipulated the chromosomalvacAgene in twoH. pyloristrains to introduce alterations in the region encoding the VacA i-region. We did not detect any differences in the capacity of i1 and i2 forms of VacA to cause vacuolation of RK13 cells. In comparison to i1 forms of VacA, i2 forms of VacA had a diminished capacity to inhibit the activation of nuclear factor of activated T cells (NFAT) and suppress interleukin-2 (IL-2) production. Correspondingly, i2 forms of VacA bound to Jurkat cells less avidly than did i1 forms of VacA. These results indicate that the VacA i-region is an important determinant of VacA effects on human T cell function.

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“…VacA behaves as a passive urea transporter and, thus, it increases the permeability of the epithelium to urea, which is broken into intermediate toxic products. The infection by CagA positive strains is associated with more serious epithelial lesions, acute or chronic severe inflammation, possibility of peptic ulceration, and risk of gastric cancer (14)(15)(16) .…”

Section: Introductionmentioning

confidence: 99%

PREVALÊNCIA DE Helicobacter spp. EM CÃES DE CAMPO GRANDE-MS

et al. 2017

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Helicobacter spp. is a spiral Gram-negative bacterium that has substantial clinical importance. It has been related to diseases such as gastritis and peptic ulcers, and more recently to gastric cancer in humans. Evidence suggests the potential of animals, particularly domestic ones, as the source of zoonotic infection of helicobacteria since bacteria with similar morphology to those found in animals were observed in the stomach of humans with gastritis. Thus, dogs have been identified to serve as an important host for infectious agents such as Helicobacter spp. From this perspective, the present study aimed to assess the prevalence of Helicobacter spp. in dogs from the Zoonosis Control Center of Campo Grande-MS. Samples of body, fundus, and gastric antrum from 96 dogs were collected to evaluate the presence of Helicobacter spp. through the rapid urease test and histological analysis. Helicobacter spp. was found in 94.7% of the dogs by rapid urease test and in 100% by histological analysis, with bacteria predominance in the stomach fundus region. Keywords: dogs; Helicobacter; urease test. ResumoA Helicobacter spp. é uma bactéria Gram negativa espiralada, de grande importância clínica, que se relaciona a patogenias como gastrite e úlceras pépticas e, mais recentemente, com o carcinoma gástrico em humanos. Evidências sugerem o potencial dos animais, principalmente os domésticos, como fonte de infecção zoonótica das helicobactérias, já que bactérias com morfologia similar às encontradas em animais foram observadas no estômago de humanos com gastrite. Nesse contexto, os cães podem ser um importante reservatório de agentes infecciosos como a Helicobacter spp. O presente trabalho teve como objetivo avaliar a prevalência de Helicobacter spp. em cães do Centro de Controle de Zoonoses de Campo Grande/MS. Para tanto, foram utilizados 96 cães dos quais foram colhidas amostras do corpo, fundo e antro gástrico, para avaliação da presença da Helicobacter spp. por meio do teste rápido de urease e análise histológica. O teste rápido de urease permitiu a detecção de Helicobacter spp. em 94,7% dos cães; já a análise histológica indicou a presença de Helicobacter spp. em 100% dos animais avaliados com predominio da bactéria na 2

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Helicobacter pylori VacA Induces Programmed Necrosis in Gastric Epithelial Cells

Cited by 100 publications

References 78 publications

Low-density Lipoprotein Receptor-related Protein-1 (LRP1) Mediates Autophagy and Apoptosis Caused by Helicobacter pylori VacA

Low-density Lipoprotein Receptor-related Protein-1 (LRP1) Mediates Autophagy and Apoptosis Caused by Helicobacter pylori VacA

The Intermediate Region of Helicobacter pylori VacA Is a Determinant of Toxin Potency in a Jurkat T Cell Assay

PREVALÊNCIA DE Helicobacter spp. EM CÃES DE CAMPO GRANDE-MS

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