Putative effect of<i>Helicobacter pylori</i>and gastritis on gastric acid secretion in cat

Sobhani, Iradj; Cañedo, S; Alchepo, Beatriz; Vissuzaine, C; Chevalier, Catherine; Buyse, Marion; Moizo, L.; Laigneau, Jean–Pierre; Mignon, M; Lewin, J.; Bado, André

doi:10.1152/ajpgi.00282.2001

Cited by 6 publications

(8 citation statements)

References 45 publications

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“…Cats infected with H. pylori ss1 (a nominally cagPAI-positive but functionally cagPAI-inactive nontoxigenic [vacAs2] strain [73]) exhibit transient hypochlorhydria (65), which is analogous to the transient hypochlorhydria reported in the early stages of infection in people (31). Thus, in vivo investigation of the interplay between inflammatory mediators, bacterial products, and gastric function may be facilitated by the cat model of infection.…”

Section: Discussionmentioning

confidence: 99%

Quantitative Evaluation of Inflammatory and Immune Responses in the Early Stages of ChronicHelicobacter pyloriInfection

et al. 2003

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The early consequences of Helicobacter pylori infection and the role of bacterial virulence determinants in disease outcome remain to be established. The present study sought to measure the development of host inflammatory and immune responses and their relationship to the putative bacterial virulence factors cag pathogenicity island (cagPAI), vacA allele, and oipA in combination with bacterial colonization density in a feline model of the early stages of H. pylori infection. Gastric tissues obtained from infected and uninfected cats were evaluated for H. pylori ureB, cagPAI, vacA allele, and oipA and colonization density (urease, histology, and real-time PCR). Inflammation was assessed by measuring mRNA upregulation of gamma interferon (IFN-␥), interleukin (IL)-1␣, IL-1␤, IL-4, IL-6, IL-8, IL-10, and IL-12 p40 and histopathology. The mucosal immune response was characterized by morphometric analysis of lymphoid follicles and by differentiating lymphocyte populations with antibodies against surface markers. Infecting H. pylori strains were positive for vacAs1 but lacked cagPAI and an active oipA gene. Colonization density was uniform throughout the stomach. Upregulation of IFN-␥, IL-1␣, IL-1␤, and IL-8 and increased severity of inflammatory infiltrates and fibrosis were observed in infected cats. The median number and total area of lymphoid aggregates were 5 and 10 times greater, respectively, in the stomachs of infected than uninfected cats. Secondary lymphoid follicles in uninfected cats were rare and positive for BLA.36 and B220 but negative for CD3 and CD79␣, whereas in infected cats they were frequent and positive for BLA.36, CD79␣, and CD3 but negative for B220. Upregulation of IFN-␥, IL-1␣, IL-1␤, and IL-8 and marked hyperplasia of secondary lymphoid follicles are early consequences of H. pylori infection in cats. The response appears to be similar to that of infected people, particularly children, can develop independently of the pathogenicity factors cagPAI and oipA, and is not correlated with the degree of colonization density or urease activity.Helicobacter pylori is a gram-negative bacterium that chronically infects more than half of all people worldwide (6,66,69,75). Infection tends to begin in infancy (new infections are uncommon in adults) and is likely to last for decades (16).Over a span of 20 to 30 years, about one in six H. pyloriinfected adults in the West develops duodenal ulcers that are associated with antral predominant gastritis and increased acid secretion (18). Another smaller subset of people develop atrophy and intestinal metaplasia of the body of the stomach and go on to develop gastric carcinoma over a period of 30 to 40 years (55). While the factors determining this variable outcome are not well understood, the development of a sustained gastric inflammatory and immune response to infection appears to be pivotal for the development of disease (12,49,55,56). Chronic infection of adults with H. pylori is characterized by the infiltration of polymorphonuclear and mononuclear cells an...

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Section: Discussionmentioning

confidence: 99%

Quantitative Evaluation of Inflammatory and Immune Responses in the Early Stages of ChronicHelicobacter pyloriInfection

et al. 2003

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“…In humans it has been reported that gastric acid secretion increases 48 wk after eradication therapy, suggesting that Helicobacter inhibits acid secretion [28] . In cats, acid secretion was inhibited within 3 wk of H. pylori infection [3] . The inhibition of gastric acid secretion may also be accounted for by suppression of histidine decarboxylase (HDC) activity that is important in the pro duction of the major acid secretagogue histamine [5,29,30] .…”

Section: Discussionmentioning

confidence: 99%

“…Cou rillonMallet et al first revealed elevated concentrations of H3R agonist Nαmethylhistamine (NαMH) in the gastric mucosa of H. pylori infected patients [1,5,6] . NαMH has an indirect inhibitory effect on acid secretion by inhibiting the acid secretagogue histamine from the ECLlike ce lls [3,5] . Stimulation of H3Rs on ECLlike cells eventually inhibits histidine decarboxylase (HDC) activity [3,5] .…”

Section: Introductionmentioning

confidence: 99%

“…NαMH has an indirect inhibitory effect on acid secretion by inhibiting the acid secretagogue histamine from the ECLlike ce lls [3,5] . Stimulation of H3Rs on ECLlike cells eventually inhibits histidine decarboxylase (HDC) activity [3,5] . Down regulation of HDC causes a decrease in the amount of histamine produced and decreased acid secretion [3,5] .…”

Section: Introductionmentioning

confidence: 99%

“…Stimulation of H3Rs on ECLlike cells eventually inhibits histidine decarboxylase (HDC) activity [3,5] . Down regulation of HDC causes a decrease in the amount of histamine produced and decreased acid secretion [3,5] . Early in vivo experiments using H3R agonist Rαmethylhistamine (RαMH) also potently inhibits gastric secretion by a number of indirect stimuli [7,8] .…”

Section: Introductionmentioning

confidence: 99%

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Histamine 3 receptor activation mediates inhibition of acid secretion duringHelicobacter-induced gastritis

Zavros

Mesiwala²,

Waghray³

et al. 2010

WJGP

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AIM:To test the hypothesis that histamine 3 receptor (H3R) activation during Helicobacter infection inhibits gastric acid secretion in vivo and in vitro . METHODS:Helicobacter felis (H. felis ) infected and uninfected C57Bl/6 mice were infused with either PBS or the H3 receptor antagonist thioperamide (THIO) for 12 wk. After treatment, mice were analyzed for morpho logical changes and gastric acid content. Total RNA was prepared from the stomachs of each group and analy zed for changes in somatostatin and gastrin mRNA abundance by real timepolymerase chain reaction (RT PCR). Location of H3 receptors in the stomach was analyzed by co-localization using antibodies specific for the H3 receptor and parietal cell marker H CONCLUSION: This study shows that during H. felis infection, gastric acidity is suppressed as a consequence of an inhibitory effect on the parietal cell by H3R acti vation. The stimulation of gastric mucosal H3Rs incre ases gastrin expression and release by inhibiting release of somatostatin.

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Histamine in the control of gastric acid secretion: a topic review

Barocelli

Ballabeni

2003

Pharmacological Research

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Putative effect ofHelicobacter pyloriand gastritis on gastric acid secretion in cat

Abstract: . Putative effect of Helicobacter pylori and gastritis on gastric acid secretion in cat. Am

Cited by 6 publications

References 45 publications

Quantitative Evaluation of Inflammatory and Immune Responses in the Early Stages of ChronicHelicobacter pyloriInfection

Quantitative Evaluation of Inflammatory and Immune Responses in the Early Stages of ChronicHelicobacter pyloriInfection

Histamine 3 receptor activation mediates inhibition of acid secretion duringHelicobacter-induced gastritis

Histamine in the control of gastric acid secretion: a topic review

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