Expression of tryptophan hydroxylase in gastric mucosa in symptomatic and asymptomatic Helicobacter pylori infection

Abstract

IntroductionHelicobacter pylori infection induces clinical symptoms in 15–20% of subjects, and the reason for this variation is still not clear. The aim of the present study is to evaluate the expression of tryptophan hydroxylase (TpH-1) in gastric mucosa of patients with symptomatic and asymptomatic H. pylori infection in relation to the intensity of bacterial colonization and severity of dyspeptic symptoms.Material and methodsNinety subjects (aged 35–49 years) were enrolled in the study and separated into 3 groups of 30 subjects each. Group I – healthy volunteers without H. pylori infection, group II – subjects with asymptomatic H. pylori infection, group III – H. pylori-infected patients with dyspeptic symptoms, mainly fasting and nocturnal epigastric pain. To diagnose H. pylori infection the urea breath test (UBT-13C) and histological analysis were performed. The level of mRNA expression of tryptophan hydroxylase (TpH-1) was estimated in gastric mucosa with RT-PCR.ResultsThe expression of this enzyme in antral mucosa was 2.69 ±0.97 in group I, 2.28 ±0.69 in group II (p > 0.05) and 4.40 ±1.64 in group III (p < 0.001). The levels of expression of TpH-1 in gastric body mucosa were 2.16 ±0.70, 1.57 ±0.52 (p > 0.05) and 3.40 ±1.51 (p < 0.001), respectively. In group III a positive correlation was found between intensity of H. pylori colonization and TpH-1 expression as well as between TpH-1 expression and severity of dyspeptic symptoms.ConclusionsIncreased expression of TpH-1 in gastric mucosa plays a role in pathogenesis of chronic dyspepsia.

Mechanisms of the Epithelial–Mesenchymal Transition and Tumor Microenvironment in Helicobacter pylori-Induced Gastric Cancer

“…Helicobacter pylori (H. pylori) is a helix-shaped, Gram-negative, microaerophilic, flagellated bacterium that is capable of biofilm formation and converting from spiral to coccoid form [1][2][3][4][5][6]. It is a highly invasive microorganism responsible for one of the highest prevalences of chronic infections worldwide, even though over 80% of infected patients remain asymptomatic [7][8][9][10][11][12][13]. H. pylori pathogenesis is due to several virulence factors including urease, cytotoxin-associated gene A (CagA),…”

“…Helicobacter pylori (H. pylori) is a helix-shaped, Gram-negative, microaerophilic, flagellated bacterium that is capable of biofilm formation and converting from spiral to coccoid form [1][2][3][4][5][6]. It is a highly invasive microorganism responsible for one of the highest prevalences of chronic infections worldwide, even though over 80% of infected patients remain asymptomatic [7][8][9][10][11][12][13]. H. pylori pathogenesis is due to several virulence factors including urease, cytotoxin-associated gene A (CagA), vacuolating cytotoxin (VacA), outer inflammatory protein A (OipA), duodenal ulcer promoting gene A (DupA), neutrophil-activating protein A (NAP), heat shock proteins (Hsp10, Hsp60), and sialic acid-binding adhesin (SabA) [14][15][16][17][18][19][20][21][22][23][24].…”

Research Article <i>Helicobacter</i> <i>pylori</i> <i>vac</i>A virulence gene analysis and association with clinical and histopathological aspects in dyspeptic patients

“…It is known that lesions in the gastric mucosa are the result of the action of bacterial toxins and an increase in the host's pro-inflammatory cytokines. Numerous studies have been carried out with symptomatic and asymptomatic patients infected with positive H. pylori cagA and vacA strains and have not found a significant relationship between the presence of these virulence genes and symptomatology (Nicolescu, 2014;Roesler et al, 2014;Chojnacki et al, 2019).…”

Genes de virulência e polimorfismos gênicos ligados à suscetibilidade à infecção por Helicobacter pylori

“…Esses polimorfismos interferem, também, na atividade transcricional, o que os associa a quadros de câncer gástrico e úlcera duodenal. 9,20,21 Os polimorfismos TNFA -1031/-863/-857 estão relacionados à elevada atividade do promotor transcricional, induzem elevação nos níveis de TNF-α nas células mononucleadas periféricas do epitélio gástrico, induzem a infiltração gástrica grave, além de serem fatores de risco independentes para quadros de úlcera gástrica e úlcera duodenal sem presença de metaplasia intestinal. 9…”