Does Helicobacter pylori infection increase gastric sensitivity in functional dyspepsia?

Mearin, F; Ribot, X de; Balboa, Agustín; Salas, Antonio; Varas, Modesto; Cucala, Mercedes; Bartolomé, Rosa; Armengol, J R; Malagelada, Juan–R.

doi:10.1136/gut.37.1.47

Cited by 117 publications

(75 citation statements)

References 18 publications

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“…93 There is also no evidence that H. pylori-infected NUD patients have altered gastric visceral perception compared with uninfected NUD controls. 94 Studies have suggested that H. pylori infection is more common in NUD patients compared with asymptomatic controls, but this is not a universal finding. A review of the literature and metaanalysis suggested H. pylori was a risk factor for NUD (odds ratio (OR), 2.3; 95% confidence interval (CI), 1.9 to 2.7), 67 but the choice of control groups in some of the studies included in the review were inappropriate.…”

Section: Evidence For the Role Of H Pylori In Nudmentioning

confidence: 99%

The management of dyspepsia: a systematic review.

Delaney

Moayyedi²,

Deeks³

et al. 2000

Health Technology Assessment

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Section: Evidence For the Role Of H Pylori In Nudmentioning

confidence: 99%

The management of dyspepsia: a systematic review.

Delaney

Moayyedi²,

Deeks³

et al. 2000

Health Technology Assessment

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“…Helicobacter pylori infection has been hypothesized to be associated with an increased postprandial gastric sensitivity in FD, although no relation between H. pylori infection and gastric hypersensitivity in humans has been established [6, 7, 8]. Experimental evidence in animals suggests that the mucosal inflammatory response associated with the infection may trigger sensitization of afferent nerve endings [5, 8].…”

Section: Introductionmentioning

confidence: 99%

Gastric Perception Thresholds Are Low and Sensory Neuropeptide Levels High in <i>Helicobacter pylori-</i>Positive Functional Dyspepsia

Mönnikes

Voort

Wollenberg³

et al. 2005

Digestion

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Background and Aims: In functional dyspepsia (FD) decreased perception levels can be shown on gastric distension. Substance P (SP) and calcitonin gene-related peptide (CGRP) are involved in the sensitization of afferent neuronal pathways due to chronic inflammation. The role of Helicobacter pylori-induced gastric mucosal inflammation in the pathogenesis of FD is controversial. The aim of this study was to assess whether FD patients have altered mucosal concentrations of CGRP and SP, and to investigate whether this is associated with visceral hypersensitivity or H. pylori infection. Methods: Gastrointestinal symptoms, H. pylori status, perception thresholds at gastric balloon distension, and gastric mucosal concentrations of CGRP and SP were determined in 13 FD patients and 18 healthy controls (HC). Results: In H. pylori-positive FD patients discomfort and pain thresholds on gastric distension were lower compared to other groups. Antral mucosal levels of CGRP and SP were higher in H. pylori-positive subjects. In FD significantly negative correlations between discomfort and pain thresholds and antral mucosal concentrations of CGRP and SP were observed. Conclusions: In FD low perception thresholds on gastric distension are associated with high levels of CGRP and SP in the antrum, suggesting that sensory neuropeptides are involved in FD pathophysiology.

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“…In our microarray analysis using the stomachs of H. pyloriassociated gnotobiotic mice, the genes of the muscle cell component were also highly upregulated. The stomachs of H. pylori-infected mice exhibit inflammation, as well as disturbance in gastric emptying (15). Therefore, such abnormally thick muscle layers accompanied by inflammation may cause a failure in gastric emptying.…”

Section: Vol 77 2011 Gastrin Regulation By Lactobacilli 6969mentioning

confidence: 99%

Role of Indigenous Lactobacilli in Gastrin-Mediated Acid Production in the Mouse Stomach

Takahashi¹,

Nakano²,

Matsuoka³

et al. 2011

Appl Environ Microbiol

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It is known that the stomach is colonized by indigenous lactobacilli in mice. The aim of this study was to examine the role of such lactobacilli in the development of the stomach. For a DNA microarray analysis, germ-free BALB/c mice were orally inoculated with 10 9 CFU lactobacilli, and their stomachs were excised after 10 days to extract RNA. As a result, lactobacillus-associated gnotobiotic mice showed dramatically decreased expression of the gastrin gene in comparison to germ-free mice. The mean of the log 2 fold change in the gastrin gene was ؊4.3. Immunohistochemistry also demonstrated the number of gastrin-positive (gastrin ؉ ) cells to be significantly lower in the lactobacillus-associated gnotobiotic mice than in the germ-free mice. However, there was no significant difference in the number of somatostatin ؉ cells in these groups of mice. Consequently, gastric acid secretion also decreased in the mice colonized by lactobacilli. In addition, an increase in the expression of the genes related to muscle system development, such as nebulin and troponin genes, was observed in lactobacillus-associated mice. Moreover, infection of germ-free mice with Helicobacter pylori also showed the down-and upregulation of gastrin and muscle genes, respectively, in the stomach. These results thus suggested that indigenous lactobacilli in the stomach significantly affect the regulation of gastrinmediated gastric acid secretion without affecting somatostatin secretion in mice, while H. pylori also exerts such an effect on the stomach.The human stomach contains only a few species of bacteria if it is free from infection with Helicobacter pylori (3). During fasting, gastric juice contains only small numbers of bacteria, approximately 10 2 to 10 3 /ml, which include Streptococcus, Lactobacillus, and Veillonella. However, these bacteria are considered nonresidents that are only in transit from the oral cavity and throat (13,19). The scarcity of such bacteria in the human stomach appears to be due to the high acidity of the luminal medium.While H. pylori is a well-known pathogenic bacterium that causes peptic ulcers and cancer in the human stomach, the bacterium has also been proposed to belong to the indigenous gastric microbiota of humans from the earliest times (2). That hypothesis is supported by the fact that H. pylori is acquired in early childhood and thereafter remains stably colonizing the stomach for decades in substantial numbers. This raises questions about the role of H. pylori as the indigenous bacteria of the stomach in the physiological development and function of the organ. However, it is difficult to clarify the answers to this question by an infection study using H. pylori, because various pathogenic factors of H. pylori, such as CagA, vacuolating toxins, and urease and its metabolites, induce chronic pathological inflammation in the gastric tissue, which obscures the physiological role of H. pylori as an indigenous bacterium.In a previous study (12), we found an indigenous microbiota that predominantly consists...

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Does Helicobacter pylori infection increase gastric sensitivity in functional dyspepsia?

Cited by 117 publications

References 18 publications

The management of dyspepsia: a systematic review.

The management of dyspepsia: a systematic review.

Gastric Perception Thresholds Are Low and Sensory Neuropeptide Levels High in <i>Helicobacter pylori-</i>Positive Functional Dyspepsia

Role of Indigenous Lactobacilli in Gastrin-Mediated Acid Production in the Mouse Stomach

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