Immune responses to<i>Helicobacter pylori</i>colonization: mechanisms and clinical outcomes

Portal-Celhay, Cynthia; Perez-Perez, Guillermo I.

doi:10.1042/cs20050232

Cited by 79 publications

(39 citation statements)

References 81 publications

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“…In 10%-15% individuals this infection can lead to severe inflammation, peptic ulcer disease (10%), mucosa-associated lymphoid tissue (MALT) lymphoma (0.1%), or gastric adenocarcinoma (1%-3%)[6-9]. H. pylori induces histological gastritis associated with an infiltration of gastric mucosa with immune cells[10]. However, other microorganisms or even non-infectious agents such as corticosteroids, nonsteroidal anti-inflammatory drugs, aspirin and excessive alcohol consumption can play a role in the development of gastritis[11-13].…”

Section: Introductionmentioning

confidence: 99%

Impact ofHelicobacter pylorion the healing process of the gastric barrier

Mnich¹,

Kowalewicz-Kulbat²,

Sicińska³

et al. 2016

WJG

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AIMTo determine the impact of selected well defined Helicobacter pylori (H. pylori) antigens on gastric barrier cell turnover.METHODSIn this study, using two cellular models of gastric epithelial cells and fibroblasts, we have focused on exploring the effects of well defined H. pylori soluble components such as glycine acid extract antigenic complex (GE), subunit A of urease (UreA), cytotoxin associated gene A protein (CagA) and lipopolysaccharide (LPS) on cell turnover by comparing the wound healing capacity of the cells in terms of their proliferative and metabolic activity as well as cell cycle distribution. Toxic effects of H. pylori components have been assessed in an association with damage to cell nuclei and inhibition of signal transducer and activator of transcription 3 (STAT3) phosphorylation.RESULTSWe showed that H. pylori GE, CagA and UreA promoted regeneration of epithelial cells and fibroblasts, which is necessary for effective tissue healing. However, in vivo increased proliferative activity of these cells may constitute an increased risk of gastric neoplasia. In contrast, H. pylori LPS showed a dose-dependent influence on the process of wound healing. At a low concentration (1 ng/mL) H. pylori LPS accelerated of healing epithelial cells, which was linked to significantly enhanced cell proliferation and MTT reduction as well as lack of alterations in cell cycle and downregulation of epidermal growth factor (EGF) production as well as cell nuclei destruction. By comparison, H. pylori LPS at a high concentration (25 ng/mL) inhibited the process of wound repair, which was related to diminished proliferative activity of the cells, cell cycle arrest, destruction of cell nuclei and downregulation of the EGF/STAT3 signalling pathway.CONCLUSIONIn vivo H. pylori LPS driven effects might lead to the maintenance of chronic inflammatory response and pathological disorders on the level of the gastric mucosal barrier.

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Section: Introductionmentioning

confidence: 99%

Impact ofHelicobacter pylorion the healing process of the gastric barrier

Mnich¹,

Kowalewicz-Kulbat²,

Sicińska³

et al. 2016

WJG

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“…Besides bacterial virulence factors, host immunological factors, including humoral immune responses directed against bacterial virulence factors, are important50. H. pylori infection induces inflammation and a strong humoral immune response to a variety of H. pylori antigens51, and H. pylori antigens are therefore regarded as potential candidates for serologic biomarkers52. In our study, the adhesins were expressed at higher levels in GC-related H. pylori , suggesting that they may cause a higher host response.…”

Section: Discussionmentioning

confidence: 54%

Combination of OipA, BabA, and SabA as candidate biomarkers for predicting Helicobacter pylori-related gastric cancer

Huang

et al. 2016

Sci Rep

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Helicobacter pylori (H. pylori ) infection is a major cause of chronic gastritis and is highly related to duodenal ulcer (DU) and gastric cancer (GC). To identify H. pylori-related GC biomarkers with high seropositivity in GC patients, differences in levels of protein expression between H. pylori from GC and DU patients were analyzed by isobaric tag for relative and absolute quantitation (iTRAQ). In total, 99 proteins showed increased expression (>1.5-fold) in GC patients compared to DU patients, and 40 of these proteins were categorized by KEGG pathway. The four human disease-related adhesin identified, AlpA, OipA, BabA, and SabA, were potential GC-related antigens, with a higher seropositivity in GC patients (n = 76) than in non-GC patients (n = 100). Discrimination between GC and non-GC patients was improved using multiple antigens, with an odds ratio of 9.16 (95% CI, 2.99–28.07; p < 0.0001) for three antigens recognized. The optimized combination of OipA, BabA, and SabA gave a 77.3% correct prediction rate. A GC-related protein microarray was further developed using these antigens. The combination of OipA, BabA, and SabA showed significant improvement in the diagnostic accuracy and the protein microarray containing above antigens should provide a rapid and convenient diagnosis of H. pylori-associated GC.

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“…Helicobacter pylori colonizes the stomachs of half of the world's population and usually persists in the gastric mucosa of human hosts for decades or life [16]. Although most H. pylori-positive people are asymptomatic, the presence of H. pylori may lead to mucosal injury.…”

Section: Discussionmentioning

confidence: 98%

Alcohol Dehydrogenase (ADH) Isoenzyme Activity in the Sera of Patients with Helicobacter pylori Infection

et al. 2007

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Human gastric mucosa contains three classes of alcohol dehydrogenase (ADH) isoenzymes: I, III, and IV. Various factors have been found to influence gastric ADH activity. One of them is Helicobacter pylori infection, which is associated with gastric mucosal injury and leads to a decrease in gastric ADH activity. The aim of the study was to assess the effect of H. pylori infection on the serum activity of ADH isoenzymes. Serum samples were taken from 35 patients with H. pylori infection and from 35 healthy subjects. For measurement of class I isoenzyme activity we employed the fluorometric method, with class-specific fluorogenic substrate (4-methoxy-1-naphthaldehyde). The activities of class III and IV ADH isoenzymes were measured by the photometric method with formaldehyde and with m-nitrobenzaldehyde as substrate, respectively. Total activity of ADH was measured by a photometric method with p-nitrosodimethylaniline. The total activities of ADH and class IV isoenzyme were significantly higher in sera of patients with H. pylori infection compared to healthy subjects. The serum activity of other tested isoenzymes of ADH did not differ significantly between infected and noninfected groups. We conclude that H. pylori infection of gastric mucosa is reflected in the serum by a significant increase in class IV and total ADH activity.

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Immune responses toHelicobacter pyloricolonization: mechanisms and clinical outcomes

Cited by 79 publications

References 81 publications

Impact ofHelicobacter pylorion the healing process of the gastric barrier

Impact ofHelicobacter pylorion the healing process of the gastric barrier

Combination of OipA, BabA, and SabA as candidate biomarkers for predicting Helicobacter pylori-related gastric cancer

Alcohol Dehydrogenase (ADH) Isoenzyme Activity in the Sera of Patients with Helicobacter pylori Infection

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