Extract of Helicobacter pylori induces neutrophils to injure endothelial cells and contains antielastase activity

Takemura, Tadashi; Granger, D. Neil; Evans, David J.; Dg, Evans; Graham, D.Y.; Anderson, D. C.; Re, Wolf; Cepinskas, Gediminas; Pr, Kvietys

doi:10.1053/gast.1996.v110.pm8536858

Cited by 40 publications

(32 citation statements)

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“…Several studies have described the effect of H. pylori infection on the structure and function of endothelial cells [22][23][24][25], most focusing on the activation of leucocytes by the bacteria, resulting in leucocyte migration and attachment to the endothelial cells and subsequent disturbance of microvascular circulation [26][27][28][29][30]. In-vitro studies [31] have shown that H. pylori induced the expression of interleukin (IL)-8 in gastric endothelial cells and another study demonstrated the mechanism of H. pylori-induced neutrophildependent vascular protein leakage of the stomach, which is regarded as another indirect effect of H. pylori.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of cell proliferation and induction of apoptosis by Helicobacter pylori through increased phosphorylated p53, p21 and Bax expression in endothelial cells

Kurosawa

Miwa

Hirose

et al. 2002

Journal of Medical Microbiology

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Microcirculation plays a crucial role in mucosal physiological function as well as repair of gastric mucosal damage. Endothelial cell damage is known to disturb microcirculation and suppress angiogenesis. Therefore, the direct effect of Helicobacter pylori on endothelial cells in vitro was investigated with H. pylori water extract. The effect of H. pylori water extract on cell proliferation and apoptosis of human umbilical vein endothelial cells (HUVECs) was evaluated. The ratio of BrdU-positive HUVECs in both cagA/vacA-positive and -negative H. pylori water extract-treated groups was significantly lower at 24 h than that in the control group, but Escherichia coli water extract did not affect the proliferation of these endothelial cells. Apoptosis was induced by H. pylori water extracts after incubation for 24 h in a cagA/vacA-independent manner. In the mitochondrial permeability transition assay, tetramethylrhodamine methyl ester was accumulated in mitochondria of HUVECs. Western blot analysis showed no difference in the level of total p53 protein in H. pylori water extract-treated and non-treated cells, but the level of phosphorylated p53 protein was increased in the treated cells at 15 and 60 min after addition of the extract. Reverse transcription (RT)-PCR products for p21 and Bax were elevated in the H. pylori water extract-treated cells. p21 levels began to increase 0.5-1 h after addition of the extract, whereas Bax increased in the period 0.5-2 h. H. pylori induced a disturbance of cell proliferation and apoptosis in the vascular endothelial cells which may contribute to gastric mucosal injury and to delayed healing of gastric lesions.

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Section: Discussionmentioning

confidence: 99%

Inhibition of cell proliferation and induction of apoptosis by Helicobacter pylori through increased phosphorylated p53, p21 and Bax expression in endothelial cells

Kurosawa

Miwa

Hirose

et al. 2002

Journal of Medical Microbiology

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“…Excluding 42 participants (38 with a history of cancer, 3 hepatitis virus carriers without blood samples, and 1 who refused blood sampling after entry), the remaining 241 outpatients were analyzed. This study was approved by the Ethical Committee of Aichi Cancer Center in 1999 (Approval number [12][13][14][15][16][17][18][19][20][21][22][23]. HP infection An HP IgG antibody test, High-Molecularweight Campylobacter-Associated-Protein (HM-CAP) ELISA ("Detaminor H. pylori antibody," Enteric Products Ins., Westbury, NY) was used for the identification of HPinfected participants.…”

Section: Study Subjectsmentioning

confidence: 99%

“…Recently, it was reported that HP water extract can activate neutrophils 20) and enhance the secretion of MPO.…”

mentioning

confidence: 99%

Low Expression Myeloperoxidase Genotype Negatively Associated with Helicobacter pylori Infection

Hamajima

Matsuo

Suzuki

et al. 2001

Japanese Journal of Cancer Research

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“…[5][6][7][8][9][10][11][12] We previously reported that H pylori and NSAIDs cause neutrophils to express adhesion molecules followed by accumulation of neutrophils into the gastric mucosa. 7 8 Activated neutrophils have been suggested to injure endothelial and epithelial cells by producing active oxygen species and proteases.…”

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confidence: 99%

Helicobacter pylori infection potentiates aspirin induced gastric mucosal injury in Mongolian gerbils

Yoshida

Sugimoto²,

Hirayama³

et al. 2002

Gut

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Extract of Helicobacter pylori induces neutrophils to injure endothelial cells and contains antielastase activity

Cited by 40 publications

References 0 publications

Inhibition of cell proliferation and induction of apoptosis by Helicobacter pylori through increased phosphorylated p53, p21 and Bax expression in endothelial cells

Inhibition of cell proliferation and induction of apoptosis by Helicobacter pylori through increased phosphorylated p53, p21 and Bax expression in endothelial cells

Low Expression Myeloperoxidase Genotype Negatively Associated with Helicobacter pylori Infection

Helicobacter pylori infection potentiates aspirin induced gastric mucosal injury in Mongolian gerbils

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