Helicobacter pylori in Health and Disease

Cover, Timothy L.; Blaser, Martin J.

doi:10.1053/j.gastro.2009.01.073

Cited by 601 publications

(566 citation statements)

References 162 publications

(187 reference statements)

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“…It has been suggested that H. Pylori, which is one of the most commonly encountered infectious agents, triggers autoimmunity. This has been put forward due to the long life of H. Pylori in the host, global widespread prevalence and a complex relationship with the host immune system [6].…”

Section: The Relationship Of Systemic Lupus Erythematosus and Helicobmentioning

confidence: 99%

The Relationship of Systemic Lupus Erythematosus and Helicobacter Pylori

Yıldırım¹,

Yıldırım²

2015

Med-Science

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Systemic lupus erythematosus (SLE) is an inflammatory disease of unknown etiology. In the pathogenesis of SLE, several infectious agents have been held responsible such as cytomegalovirus, parvovirus B19 and Epstein Barr virus (EBV). There is a variable relationship between SLE and helicobacter, which is different from that of lupus and other infections. We would like to emphasize the interrelation between these entities.

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Section: The Relationship Of Systemic Lupus Erythematosus and Helicobmentioning

confidence: 99%

The Relationship of Systemic Lupus Erythematosus and Helicobacter Pylori

Yıldırım¹,

Yıldırım²

2015

Med-Science

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“…For the gastric pathogen Helicobacter pylori (Hp), chronic infection is associated with increased apoptosis within the gastric mucosa of humans (3), mice (4), and Mongolian gerbil models (5). Increased apoptosis may alter the gastric environment to promote Hp persistence (6), while at the same time, contribute to gastric disease, including peptic ulcers and gastric adenocarcinoma (7). Earlier studies have indicated that the vacuolating cytotoxin A (VacA), an Hp virulence factor that is important for Hp colonization (8) and disease pathogenesis (9), is essential (10) and sufficient (11) for inducing gastric epithelial cell death.…”

mentioning

confidence: 99%

Helicobacter pylori vacuolating cytotoxin A (VacA) engages the mitochondrial fission machinery to induce host cell death

Jain

Luo

Blanke³

2011

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

149

119

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A number of pathogenic bacteria target mitochondria to modulate the host's apoptotic machinery. Studies here revealed that infection with the human gastric pathogen Helicobacter pylori disrupts the morphological dynamics of mitochondria as a mechanism to induce host cell death. The vacuolating cytotoxin A (VacA) is both essential and sufficient for inducing mitochondrial network fragmentation through the mitochondrial recruitment and activation of dynamin-related protein 1 (Drp1), which is a critical regulator of mitochondrial fission within cells. Inhibition of Drp1-induced mitochondrial fission within VacA-intoxicated cells inhibited the activation of the proapoptotic Bcl-2-associated X (Bax) protein, permeabilization of the mitochondrial outer membrane, and cell death. Our data reveal a heretofore unrecognized strategy by which a pathogenic microbe engages the host's apoptotic machinery.cytochrome c | mitochondrial dynamics | gastric cancer | gastric ulcer | toxin

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“…Approximately 80% of the infected individuals remain asymptomatic; however, the remaining 20% of infected individuals develop chronic gastritis when left untreated [10]. H. pylori has been associated with gastric cancer, in the context of chronic infection and gastric mucosa inflammation.…”

Section: Helicobacter Pylori Alters Content and Maintenance Of The Homentioning

confidence: 99%

When our genome is targeted by pathogenic bacteria

Lemercier

2015

Cell. Mol. Life Sci.

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Eukaryotic cells repair thousands of lesions arising in the genome at each cell cycle. The most hazardous damage is likely DNA doublestrand breaks (DSB) that cleave the double helix backbone. DSBs occur naturally during T-cell receptor and immunoglobulin gene recombination in lymphocytes. DSBs can also arise as a consequence of exogenous stresses (e.g. ionizing irradiation, chemotherapeutic drugs, viruses) or oxidative processes. An increasing number of studies have reported that infection with pathogenic bacteria also alters the host genome, producing DSB and other modifications on DNA. This review focuses on recent data on bacteria-induced DNA damage and the known strategies used by these pathogens to maintain a physiological niche in the host. Even after DNA repair in infected cells, "scars" often remain on chromosomes and might generate genomic instability at the next cell division. Chronic inflammation in tissue, combined with infection and DNA damage, can give rise to genomic instability and eventually cancer. A functional link between the DNA damage response and the innate immune response has been recently established. Pathogenic bacteria also highjack the host cell cycle, often acting on the stability of the master regulator p53, or dampen the DNA damage response to support bacterial replication in an appropriate reservoir. Except in a few cases, the molecular mechanisms responsible for DNA lesions are poorly understood, although ROS release during infection is a serious candidate for generating DNA breaks. Thus, chronic or repetitive infections with genotoxic bacteria represent a common source of DNA lesions that compromise host genome integrity.

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Helicobacter pylori in Health and Disease

Cited by 601 publications

References 162 publications

The Relationship of Systemic Lupus Erythematosus and Helicobacter Pylori

The Relationship of Systemic Lupus Erythematosus and Helicobacter Pylori

Helicobacter pylori vacuolating cytotoxin A (VacA) engages the mitochondrial fission machinery to induce host cell death

When our genome is targeted by pathogenic bacteria

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