Expression of Tumor Necrosis Factor–α–Related Apoptosis‐Inducing Ligand and Its Proapoptotic Receptors Is Down‐Regulated during Gastric Infection with VirulentcagA⁺/vacAs1⁺Helicobacter pyloriStrains

Abstract

Down-regulation of the TRAIL system, in the context of H. pylori infection, may limit exaggerated apoptosis of gastric epithelial cells and destruction of tissue and, therefore, may enable H. pylori to maintain its niche.

Helicobacter pylori‐induced apoptosis in T cells is mediated by the mitochondrial pathway independent of death receptors

“…One model of H. pylori -induced gastric carcinogenesis proposes that apoptosis of mucosal cells leads to a compensatory epithelial cell proliferation [6,7]. So far, the mechanisms T-cell apoptosis induced by H. pylori are not fully understood [10]. The loss of immunocompetent, cells due to H. pylori -induced apoptosis could explain the impaired or inappropriate host T-cell response in the gastric mucosa towards H. pylori .…”

“…The loss of immunocompetent, cells due to H. pylori -induced apoptosis could explain the impaired or inappropriate host T-cell response in the gastric mucosa towards H. pylori . So far, the mechanisms T-cell apoptosis induced by H. pylori are not fully understood [10]. Moreover, it is still unclear how H. pylori , despite inducing a local and systemic immune response, can evade the immune system [11].…”

Acetylation of Apurinic/Apyrimidinic Endonuclease-1 Regulates Helicobacterpylori-Mediated Gastric Epithelial Cell Apoptosis

“…Interplay between bacterial factors and host signal transduction pathways determine host cell apoptotic or antiapoptotic events 4, 5 . H. pylori -mediated apoptosis involves activation of MHC class II,6 p53,7 Fas/FasL system,8 and TNF-related apoptosis inducing ligand (TRAIL) 9 . H. pylori enhance Bax expression10 and mitochondrial translocation leading to GEC death 11.…”

Helicobacter pylori Strikes Again

“…For example, it has been shown that infection of the gastric mucosa with H. pylori leads to increased apoptosis of the gastric epithelial cells, which enhances antigen survival (Neu et al, 2005). The cytotoxin associated gene A (cagA) is a particular strain of H. pylori thought by some researchers to be particularly virulent and proinflammatory.…”