<i>Helicobacter pylori </i>induced apoptosis

Shirin, Haim; Sf, Moss

doi:10.1136/gut.43.5.592

Cited by 79 publications

(73 citation statements)

References 27 publications

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“…Increased TNF-α secretion is associated with an increased level of apoptosis (18), independent of expression of the vacuolating cytotoxin (32) or the cagA status (25) of H. pylori. Apoptosis has been recognized as a factor in H. pylori-related mucosal injury (11,13,23,28,38). We therefore hypothesized that there was a reduced mucosal inflammatory response due to the loss of TNF-α in TNF-α-deficient mice.…”

Section: Discussionmentioning

confidence: 99%

Role of Tumor Necrosis Factor‐Alpha and Interferon‐Gamma in Helicobacter pylori Infection

Yamamoto

Kita

Ohno

et al. 2004

Microbiology and Immunology

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Immune responses to Helicobacter pylori infection play important roles in gastroduodenal diseases. The contributions of tumor necrosis factor‐α (TNF‐α) and interferon‐7 (IFN‐γ) to the induction of gastric inflammation and to the protection from H. pylori infection were investigated using TNF‐α gene‐knockout (TNF‐α−/−) mice and IFN‐γ gene‐knockout (IFN‐γ−/−) mice. We first examined the colonizing ability of H. pylori strain CPY2052 in the stomach of C57BL/6 wild‐type and knockout mice. The number of H. pylori colonized in the stomach of IFN‐γ−/− and TNF‐α−/− mice was higher than that of wild‐type mice. These findings suggest that TNF‐α and IFN‐γ may play a protective role in H pylori infection. Furthermore, we examined the contribution of TNF‐α and IFN‐γ to gastric inflammation. The CPY2052‐infected TNF‐α−/− mice showed a moderate infiltration of mononuclear cells in the lamina propria and erosions in the gastric epithelium as did wild‐type mice, whereas the CPY2052‐infected IFN‐γ−/− mice showed no inflammatory findings even 6 months after infection. These results demonstrate that IFN‐γ may play an important role in gastric inflammation induced by H. pylori infection, whereas TNF‐α may not participate in the development of inflammatory response.

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Section: Discussionmentioning

confidence: 99%

Role of Tumor Necrosis Factor‐Alpha and Interferon‐Gamma in Helicobacter pylori Infection

Yamamoto

Kita

Ohno

et al. 2004

Microbiology and Immunology

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“…Infiltration of the intestinal mucosa by polymorphonuclear leukocytes (PMNL), which is associated with epithelial apoptosis, occurs commonly in gastrointestinal infections (Iwamoto et al ., 1996;Shirin & Moss, 1998). The exact role of PMNL/heterophils in the pathogenesis of epithelial apoptosis is not clear.…”

Section: Discussionmentioning

confidence: 99%

“…These progenitor cells proliferate and differentiate while migrating to the tip of the villus, where they undergo physiological apoptosis (Pritchard & Watson, 1996). While apoptosis is a normal process in intestine mucosal epithelium cell turnover, it also plays an important role in the pathogenesis of several gastrointestinal diseases, such as those caused by rotavirus infection and in ulcerative colitis (Iwamoto et al ., 1996;Shirin & Moss, 1998;Boshuizen et al ., 2003). A disturbance in stem cell proliferation, apoptosis or epithelial cell turnover is common to the pathogenesis of most gastrointestinal tract infections (Guy-Grand et al ., 1998).…”

Section: Introductionmentioning

confidence: 99%

The pathogenesis of and susceptibility to malabsorption syndrome in broilers is associated with heterophil influx into the intestinal mucosa and epithelial apoptosis

et al. 2005

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Malabsorption syndrome (MAS) in broilers is characterized by enteritis and reduced body weight gain. The pathogenesis of the intestinal lesions and the reasons for susceptibility differences between broiler lines are not clear. We studied the development of enteric lesions, epithelial apoptosis, and cell proliferation in relation to susceptibility. One-day-old chickens from two broiler lines were orally inoculated with intestinal homogenate derived from MAS-affected chickens. Vacuolar degeneration and apoptosis of the villous epithelium and infiltration of heterophils into the lamina propria occurred from day 1 post-inoculation. Following heterophil accumulation, at day 4 to 6 post-inoculation, there was severe apoptosis of the crypt epithelium and villous atrophy. The susceptible broilers had a significantly greater influx of heterophils and, subsequently, severe epithelial apoptosis and cystic damage to the crypts. There appeared to be a causal relationship between heterophil influx and the onset of apoptosis. Coincident with the epithelial apoptosis, MAS-affected chickens had crypt hyperproliferation and faster epithelial turnover. Heterophil infiltration and epithelial apoptosis appear to be critical in the pathogenesis of MAS. Heterophil recruitment may be a major factor in differences in susceptibility to MAS.

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“…Normally, the gut mucosa is maintained by regular renewal of the surface epithelium by proliferation of stem cells at the base of crypts, migrating of these cells to the tip of the villus, and then apoptosis (Pritchard and Watson, 1996;Mayhew et al, 1999). A disturbance of this regular intestinal renewal, stem cell proliferation and apoptosis, could lead to intestinal damage as is shown for different gastrointestinal tract diseases as rotavirus infection and ulcerative colitis (Iwamoto et al, 1996;Guy-Grand et al, 1998;Shirin and Moss, 1998;Boshuizen et al, 2003). A disturbance in maintenance of the intestine by apoptosis and proliferation could play a role in the pathogenesis of the mucosal lesions in MAS.…”

Section: Pathogenesismentioning

confidence: 99%