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Studies on the gastric mucosal microcirculation. 2. Helicobacter pylori water soluble extracts induce platelet aggregation in the gastric mucosal microcirculation in vivo.

ABSTRACT: BACKGROUND: The exact mechanisms by which Helicobacter pylori infection results in gastric mucosal injury are unclear. AIMS: To assess in vivo whether H pylori extracts could initiate an inflammatory response in the rat gastric mucosal microcirculation. METHODS: Extracts of H pylori, Escherichia coli, or distilled water were administered topically to the gastric mucosa of anaesthetised animals. Fluorescence in vivo microscopy assessed macromolecular leakage of labelled albumin from mucosal vessels, leucocyte adherence/rolling, and platelet activity for 90 minutes. RESULTS: H pylori induced increases (p < 0.001) in adherent platelet thrombi and circulating platelet emboli after five and 15 minutes respectively. Adherent platelet thrombi (mean of four per field of view) remained significantly increased throughout the experiment, but circulating emboli (maximum of five at 30 minutes) decreased with time. Leucocyte adherence did not occur although early transient rolling was observed. An 11% increase (p < 0.02) in albumin leakage occurred after five minutes only. The induction of platelet aggregation was only observed following H pylori administration. CONCLUSION: This in vivo study demonstrated the ability of H pylori extracts to promote platelet aggregation within gastric mucosal microvessels. Recruitment of leucocytes was not observed. The results suggest that the early events associated with H pylori infection are platelet aggregation with perhaps subsequent leucocyte recruitment by activated platelets.

SUBMITTER: Kalia N

PROVIDER: S-EPMC1891607 | biostudies-other | 1997 Dec

REPOSITORIES: biostudies-other

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Age and Helicobacter pylori decrease gastric mucosal surface hydrophobicity independently.

Project description:BACKGROUND: Gastric mucosal surface hydrophobicity (GMSH) is an essential component of the mucosal defence system that is decreased by Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs). Gastric ulcers occur predominantly in elderly subjects, and may thus reflect diminished mucosal resistance. AIMS: To investigate whether aging decreases GMSH. PATIENTS: One hundred and twenty patients without peptic ulcer disease were divided into three age groups: I (41 years or below); II (41-64 years); and III (65 years or above). METHODS: Biopsy specimens were taken from the antrum, corpus, and cardia for histology (Sydney system), urease testing for H pylori, and for contact angle measurement of GMSH with a goniometer. The presence of specific H pylori antibodies was checked by immunoblotting. RESULTS: Fifty two patients (43%) were infected, and 68 were uninfected with H pylori. GMSH at all biopsy sites was lower in H pylori infected subjects (p=0.0001), but also decreased with age independently of infection status (p=0.0001). The most notable decrease in GMSH occurred between age groups I and II in those with, and between age groups II and III in those without, H pylori infection. GMSH was greater in antral than in corpus mucosa in both infected (p=0.0001) and uninfected patients (p=0.0003). CONCLUSIONS: A physiological decrease in GMSH with aging may contribute to the risk of ulcer development in the elderly, and may act synergistically with H pylori and/or NSAIDs on gastric mucosal defence.

| S-EPMC1727283 | biostudies-other

A Possible Link between Gastric Mucosal Atrophy and Gastric Cancer after Helicobacter pylori Eradication.

Project description:BackgroundThe effect of H. pylori eradication in gastric cancer prevention can be attributed to the improvement of atrophic gastritis, which is a known risk of gastric cancer. However, gastric cancer has also been diagnosed after long-term H. pylori eradication. This study aimed to clarify the association between gastric atrophy and gastric cancer after H. pylori eradication, including its clinicopathological features.MethodsA total of 55 consecutive patients with 64 early gastric cancers (EGCs) diagnosed after H. pylori eradication were enrolled. The degree of endoscopic atrophy and the histological degrees of mononuclear cell infiltration, atrophy, and metaplasia in the corpus and adjacent mucosa of the EGCs were determined and scored.ResultsThe majority of EGCs (63/64) were located within the endoscopically assessed atrophic mucosa or along the atrophic border. The adjacent mucosa of the EGCs presented significantly higher degrees of all histological parameters than in the corpus (mononuclear cell infiltration, 0.86+/-0.09 vs. 0.51+/-0.11, P = 0.016; atrophy, 1.77+/-0.13 vs. 0.65+/-0.14, P<0.0001; metaplasia, 1.68+/-0.13 vs. 0.48+/-0.1, P<0.0001). The degree of endoscopic atrophy improved in the patients with longer post-H. pylori eradication periods; however, this trend was not observed for the histological parameters, and high degrees of atrophy and metaplasia were observed in the adjacent mucosa of the EGCs compared with the corpus during all periods (all P<0.05). The histological degrees of atrophy and metaplasia in the adjacent mucosa were particularly higher in the patients who underwent eradication due to gastric ulcers.ConclusionsSevere gastric atrophy remained in the adjacent mucosa of the EGCs after H. pylori eradication, which may be linked to gastric carcinogenesis.

| S-EPMC5051933 | biostudies-literature

Gastric low-grade mucosal-associated lymphoid tissue-lymphoma: Helicobacter pylori and beyond.

Project description:The stomach is the most frequently involved site for extranodal lymphomas, accounting for nearly two-thirds of all gastrointestinal cases. It is widely accepted that gastric B-cell, low-grade mucosal-associated lymphoid tissue (MALT)-lymphoma is caused by Helicobacter pylori (H. pylori) infection. MALT-lymphomas may engender different clinical and endoscopic patterns. Often, diagnosis is confirmed in patients with only vague dyspeptic symptoms and without macroscopic lesions on gastric mucosa. H. pylori eradication leads to lymphoma remission in a large number of patients when treatment occurs at an early stage (I-II(1)). Neoplasia confined to the submucosa, localized in the antral region of the stomach, and without API2-MALT1 translocation, shows a high probability of remission following H. pylori eradication. When both bacterial infection and lymphoma recur, further eradication therapy is generally effective. Radiotherapy, chemotherapy and, in selected cases, surgery are the available therapeutic options with a high success rate for those patients who fail to achieve remission, while data on immunotherapy with monoclonal antibodies (rituximab) are still scarce. The 5-year survival rate is higher than 90%, but careful, long-term follow-up is required in these patients since lymphoma recurrence has been reported in some cases.

| S-EPMC2998825 | biostudies-literature

Helicobacter pylori chronic infection and mucosal inflammation switches the human gastric glycosylation pathways.

Project description:Helicobacter pylori exploits host glycoconjugates to colonize the gastric niche. Infection can persist for decades promoting chronic inflammation, and in a subset of individuals lesions can silently progress to cancer. This study shows that H. pylori chronic infection and gastric tissue inflammation result in a remodeling of the gastric glycophenotype with increased expression of sialyl-Lewis a/x antigens due to transcriptional up-regulation of the B3GNT5, B3GALT5, and FUT3 genes. We observed that H. pylori infected individuals present a marked gastric local pro-inflammatory signature with significantly higher TNF-? levels and demonstrated that TNF-induced activation of the NF-kappaB pathway results in B3GNT5 transcriptional up-regulation. Furthermore, we show that this gastric glycosylation shift, characterized by increased sialylation patterns, favors SabA-mediated H. pylori attachment to human inflamed gastric mucosa. This study provides novel clinically relevant insights into the regulatory mechanisms underlying H. pylori modulation of host glycosylation machinery, and phenotypic alterations crucial for life-long infection. Moreover, the biosynthetic pathways here identified as responsible for gastric mucosa increased sialylation, in response to H. pylori infection, can be exploited as drug targets for hindering bacteria adhesion and counteract the infection chronicity.

| S-EPMC4638172 | biostudies-literature

Gastric mucosal interleukin-17 and -18 mRNA expression in Helicobacter pylori-induced Mongolian gerbils.

Project description:Helicobacter pylori infection causes characteristic mucosal infiltration of inflammatory cells, resulting in the development of peptic ulcers and gastric cancer in approximately 10% of cases. Different clinical expressions of the infection may reflect different patterns of cytokine expression. Interleukin (IL)-1ss, tumor necrosis factor (TNF)-alpha, IL-17, and IL-18 have been reported to be involved in H. pylori-induced gastric mucosal inflammation, but the details and relation to different patterns of inflammation remain unclear. Moreover, the proinflammatory virulence factor outer inflammatory protein (OipA) was reported to be associated with gastric mucosal inflammatory cytokine levels. To clarify these findings, Mongolian gerbils were infected for up to 12 months with wild-type H. pylori 7.13 or with isogenic oipA mutants for 3 months, and mucosal cytokines (IL-1ss, IL-17, IL-18, and TNF-alpha) mRNA levels were then assessed using real-time RT-PCR. Antral mucosal IL-1beta and IL-18 mRNA levels peaked 1 month after infection, whereas the peak of TNF-alpha mRNA was at 6-12 months; IL-17 levels peaked at 12 months. The inflammatory cell infiltration and mRNA levels of all cytokines studied were significantly lower in oipA mutants than in wild-type-infected gerbils. Mucosal IL-1ss, IL-17, and TNF-alpha expression, but not that of IL-18, were significantly associated with the grade of inflammatory cell infiltration. The pattern of increased inflammatory cytokines differed relative to the phase of the infection and pattern of inflammation. OipA appears to play a role in IL-1ss, IL-17, and TNF-alpha expression and the resulting inflammation.

| S-EPMC3128813 | biostudies-literature

Gastric mucosal status in populations with a low prevalence of Helicobacter pylori in Indonesia.

Project description:In Indonesia, endoscopy services are limited and studies about gastric mucosal status by using pepsinogens (PGs) are rare. We measured PG levels, and calculated the best cutoff and predictive values for discriminating gastric mucosal status among ethnic groups in Indonesia. We collected gastric biopsy specimens and sera from 233 patients with dyspepsia living in three Indonesian islands. When ?5.5 U/mL was used as the best cutoff value of Helicobacter pylori antibody titer, 8.6% (20 of 233) were positive for H. pylori infection. PG I and II levels were higher among smokers, and PG I was higher in alcohol drinkers than in their counterparts. PG II level was significantly higher, whereas PG I/II ratios were lower in H. pylori-positive than in H. pylori-negative patients. PG I/II ratios showed a significant inverse correlation with the inflammation and atrophy scores of the antrum. The best cutoff values of PG I/II were 4.05 and 3.55 for discriminating chronic and atrophic gastritis, respectively. PG I, PG II, and PG I/II ratios were significantly lower in subjects from Bangli than in those from Makassar and Surabaya, and concordant with the ABC group distribution; however, group D (H. pylori negative/PG positive) was the lowest in subjects from Bangli. In conclusion, validation of indirect methods is necessary before their application. We confirmed that serum PG level is a useful biomarker determining chronic gastritis, but a modest sensitivity for atrophic gastritis in Indonesia. The ABC method should be used with caution in areas with a low prevalence of H. pylori.

| S-EPMC5413002 | biostudies-literature

Natural history of gastric mucosal cytokine expression in Helicobacter pylori gastritis in Mongolian gerbils.

Project description:Data regarding the chronological changes in gastric mucosal cytokines in the different phases of Helicobacter pylori infection are unavailable. We examined Mongolian gerbils for up to 52 weeks after H. pylori (ATCC 43504) inoculation. Levels of mRNAs of mucosal cytokines (interleukin-1beta [IL-1beta], gamma interferon [IFN-gamma], IL-4, IL-6, and IL-10) were assessed using real-time reverse transcription-PCR. Starting 26 weeks after H. pylori inoculation, two clinicohistologic patterns appeared: gastric ulcers in 32% and hyperplastic polyps in 68% of gerbils. High levels of mucosal IL-1beta mRNA were observed early in the infection, reaching maximum at 4 weeks and then rapidly declining. Mucosal IFN-gamma mRNA also reached maximal levels at 4 weeks but remained high thereafter. Both IL-1beta and IFN-gamma mRNA levels were consistently higher in the pyloric mucosa than in the fundic mucosa. In contrast, IL-4, IL-6, and IL-10 mRNA levels peaked at 8 to 26 weeks and levels were similar in the pyloric mucosa and the fundic mucosa. IFN-gamma mRNA levels were significantly higher in gerbils with ulcers than in those with hyperplastic polyps (median IFN-gamma/glyceraldehyde-3-phosphate dehydrogenase ratio x 100,000 = 650 versus 338, respectively [antrum], and 172 versus 40, respectively [corpus]) (P < 0.05). We propose that the different outcomes (e.g., ulcers or hyperplastic polyps) might relate to imbalances among cytokines.

| S-EPMC1087449 | biostudies-literature

Helicobacter pylori in gastric carcinogenesis.

Project description:Gastric cancer still is a major concern as the third most common cancer worldwide, despite declining rates of incidence in many Western countries. Helicobacter pylori (H. pylori) is the major cause of gastric carcinogenesis, and its infection insults gastric mucosa leading to the occurrence of atrophic gastritis which progress to intestinal metaplasia, dysplasia, early gastric cancer, and advanced gastric cancer consequently. This review focuses on multiple factors including microbial virulence factors, host genetic factors, and environmental factors, which can heighten the chance of occurrence of gastric adenocarcinoma due to H. pylori infection. Bacterial virulence factors are key components in controlling the immune response associated with the induction of carcinogenesis, and cagA and vacA are the most well-known pathogenic factors. Host genetic polymorphisms contribute to regulating the inflammatory response to H. pylori and will become increasingly important with advancing techniques. Environmental factors such as high salt and smoking may also play a role in gastric carcinogenesis. It is important to understand the virulence factors, host genetic factors, and environmental factors interacting in the multistep process of gastric carcinogenesis. To conclude, prevention via H. pylori eradication and controlling environmental factors such as diet, smoking, and alcohol is an important strategy to avoid H. pylori-associated gastric carcinogenesis.

| S-EPMC4678392 | biostudies-literature

Non-<i>pylori Helicobacters</i> (NHPHs) Induce Shifts in Gastric Microbiota in <i>Helicobacter pylori</i>-Infected Patients.

Project description:To explore the effects of gastric non-H. pylori Helicobacter species(NHPH) on the structure and potential function of gastric microbiota, we employed 16S rRNA gene sequencing on 164 gastric biopsy specimens from NHPH (H. suis, H. felis, H. salomonis) /H. pylori coinfection individuals, H. pylori monoinfection individuals and healthy controls. The results demonstrated that marked structural and functional variations between H. pylori mono- and coinfection samples (HPHS, HPHF, HPHM). The changes in bacterial structure induced by NHPH are mainly attributed to their ability of gastric acid secretion inhibition as well as bacterial chemotaxis. Both the HPHS and HPHF groups showed significant increases in phylotype richness and significant decreases in β diversity, but this trend was not found in HPHM group. Regarding the top five phyla and top thirty-five genera, the HPHS and HPHF groups had similar variation trends in relative abundance. The increased relative abundance levels of the genera Vibrio, Pseudoalteromonas, Photobacterium, and Clostridium were associated with increases in predicted signal transduction/metabolic pathways among the three coinfection groups. The relative abundance levels of bacteria involved in the formation of N-nitroso compounds were significantly decreased in the HPHS and HPHF groups (e.g., Streptococcus, Neisseria, Haemophilus, Veillonella, Clostridium, etc.). The significantly decreased relative abundance levels of the phyla Firmicutes and Bacteroidetes in the HPHS and HPHF groups were associated with the observed increases in predicted lipid metabolism pathways. The results in this study implied that NHPH can arouse the variation of structure and function of gastric microbiota, which may pave the way to further research on the pathogenesis of gastric diseases.

| S-EPMC5462978 | biostudies-literature

Non-Helicobacter pylori Helicobacter (NHPH) positive gastric cancer.

Project description:Genetic analysis and culturing techniques for gastric non-Helicobacter pylori Helicobacter (NHPH) are progressing. NHPH is reported to accompany nodular gastritis, gastric MALT lymphoma, and mild gastritis. However, only a few gastric cancer cases infected by NHPH have been reported. PCR analysis specific for NHPH and H. pylori was performed for DNA from gastric mucosa of 282 Korean gastric cancer patients, who were treated with endoscopic submucosal dissection. For more precise strain detection of NHPH, NHPH-positive mucosa was stained by immunohistochemistry specific for Helicobacter suis. The Cancer Genome Atlas (TCGA) classification was analyzed for these 3 gastric cancer sub-groups by in situ hybridization and immunohistochemistry. Among 281 patients, 3 patients (1.1%) were positive for NHPH. One patient (Patient 1) was also positive for H. pylori by PCR, another patient (Patient 3) was positive for serum IgG for H. pylori, and the other patient (Patient 2) had no evidence for H. pylori infection. Gastric mucosa of Patients 2 and 3 were positive for H. suis staining. All three NHPH-positive gastric cancers were located in the antrum, and belonged to the Chromosomal Instability Type of TCGA classification. Gastric NHPH can be a cause of gastric cancer, although likely with lower pathogenesis than H. pylori.

| S-EPMC8938428 | biostudies-literature

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