scholarly journals Duodenal ulcer promoting gene (DupA), plasticity region genes and sigma factors in H. pyloristrains from Nigeria

2020 ◽  
Vol 14 (02) ◽  
pp. 162-168
Author(s):  
Tolulope Funbi Jolaiya ◽  
Muinah Adenike Fowora ◽  
Charles Onyekwere ◽  
Rose Ugiagbe ◽  
Ifeanyi Ifeoma Agbo ◽  
...  

Introduction: Helicobacter pylori is a principal cause of gastric cancer. The aim of this study was to determine the prevalence and contribution of duodenal ulcer promoting gene A (dupA), the plasticity region genes and sigma factors in relation to their pathological expression of H. pylori infections in the Nigerian population. Methodology: Polymerase Chain Reaction was used to analyze a total of forty-nine H. pylori strains isolated from patients attending various endoscopic units in tertiary hospitals in Nigeria for complete dupA (G27 variant), jhp0917, jhp0918, other plasticity region genes jhp 914/917, jhp0914, jhp0940 and sigma factors. Results: PCR results indicated that the prevalence of complete dupA (G27 variants), jhp0917, jhp0918 and other plasticity region genes jhp0914, jhp0914/0917 and jhp0940 in the H. pylori strains were 4%, 53%, 88%, 73%, 12% and 0% respectively. The prevalence values of the sigma factors were 96%, 92%, 80% for rpoN,  fliA and rpoD respectively. However, the endoscopic findings showed that erosion, normal mucosal, ulcer, hyperaemic stomach, mucosal atrophy and oedematous stomach in the patients where the H. pylori strains were isolated were 40.8%, 32.7%, 10.2%, 8.2%, 2.0% and 6.1% respectively. There was significant association between jhp0917, jhp914/917 and G27 variant and the endoscopic findings, while other plasticity genes showed no association with the endoscopic findings. Conclusion: These results suggest that the presence of jhp0917, jhp0914/917 and G27 variant could be used as marker to predict the pathological effect of severity in Nigeria patients with H. pylori infection.

Blood ◽  
2001 ◽  
Vol 98 (4) ◽  
pp. 1182-1187 ◽  
Author(s):  
Hongxiang Liu ◽  
Hongtao Ye ◽  
Ahmet Dogan ◽  
Renzo Ranaldi ◽  
Rifat A. Hamoudi ◽  
...  

The development of gastric mucosa-associated lymphoid tissue (MALT) lymphoma is a multistep process and can be clinico-pathologically divided into Helicobacter pylori-associated gastritis, low-grade tumors, and high-grade tumors. The molecular events underlying this progression are largely unknown. However, identification of the genes involved in MALT lymphoma-specific t(11;18)(q21;q21) and t(1;14)(p22;q32) has provided fresh insights into the pathogenesis of this disease. T(11;18)(q21;q21) results in a chimeric transcript between the API2 and theMALT1 genes, whereas t(1;14) (p22;q32) causes aberrant nuclear BCL10 expression. Significantly, nuclear BCL10 expression also occurs frequently in MALT lymphomas without t(1;14)(p22;q32), suggesting an important role for BCL10 in lymphoma development. Thirty-three cases of H pylori gastritis, 72 MALT lymphomas, and 11 mucosal diffuse large B-cell lymphomas (DLBCL) were screened for t(11;18)(q21;q21) by reverse transcription–polymerase chain reaction followed by sequencing. BCL10 expression in lymphoma cases was examined by immunohistochemistry. The API2–MALT1 fusion transcript was not detected in H pylorigastritis and mucosal DLBCL but was found in 25 of 72 (35%) MALT lymphomas of various sites. Nuclear BCL10 expression was seen in 28 of 53 (53%) of MALT lymphomas. Of the gastric cases, the largest group studied, the frequency of both t(11;18)(q21;q21) and nuclear BCL10 expression was significantly higher in tumors that showed dissemination to local lymph nodes or distal sites (14 of 18 = 78% and 14 of 15 = 93%, respectively) than those confined to the stomach (3 of 29 = 10% and 10 of 26 = 38%). Furthermore, t(11;18)(q21;q21) closely correlated with BCL10 nuclear expression. These results indicate that both t(11;18)(q21;q21) and BCL10 nuclear expression are associated with advanced MALT lymphoma and that their oncogenic activities may be related to each other.


Author(s):  
Anja Šterbenc ◽  
Maja M. Lunar ◽  
Matjaž Homan ◽  
Boštjan Luzar ◽  
Nina Zidar ◽  
...  

Various polymerase chain reaction- (PCR-) based methods with varying positivity rates were designed to detect the Helicobacter pylori babA2 gene. To compare different primer sets, babA2 prevalence was determined in 279 H. pylori-positive pediatric samples using the 832 bp, 139 bp, and 271 bp PCR primer sets, resulting in 34.0%, 51.3%, and 79.6% prevalence of the babA2 gene, respectively. The babA2 status determined using the 832 bp and 139 bp PCR primer sets significantly correlated with bacterial density and activity of inflammation, whereas no such correlations were found using the 271 bp PCR primer set. The 139 and 832 bp PCR primer sets concordantly detected the babA2 gene in 93 cases; however, in comparison to the 832 bp PCR primer set, the 139 bp PCR primer set detected additional 50 babA2 cases, whereas only two 832 bp positive cases were missed. The 271 bp PCR primer set missed 32 babA2 cases that were 832 bp and/or 139 bp PCR positive, but tested solely positive in 109 cases. Interestingly, cloning of a subset of 271 bp PCR positive samples revealed amplification of the babA/B gene chimera. Hence, in our opinion, the 271 bp PCR protocol is not a reliable diagnostic tool for detecting the babA2 gene in children. Our results reaffirm previous observations that the use of certain babA2 PCR primer sets can significantly impact estimation of the prevalence and clinical relevance of the H. pylori babA2 gene in children, suggesting babA2 detection methods should be carefully selected.


2017 ◽  
Vol 98 (5) ◽  
pp. 723-728 ◽  
Author(s):  
A R Akhtereeva ◽  
Yu N Davidyuk ◽  
R A Faizullina ◽  
K A Ivanovskaya ◽  
A G Safin ◽  
...  

Aim. Investigation of the prevalence of various H. pylori genotypes among children and adult population of Kazan with chronic gastroduodenal pathology. Methods. The study included 107 patients (49 children and 58 adults) with chronic gastritis/gastroduodenitis and gastric and duodenal ulcer who had H. pylori infection confirmed by molecular genetic method. All patients underwent biospy from antral mucosa during endoscopy for H. pylori verification by polymerase chain reaction and genotyping for сagA and babA genes and iceA and vacA allels. Results. CagA gene was found in 19 (32.8%) out of 58 adults and 13 (26.5%) out of 49 children. VacA gene was detected in all patients (100%). VacAs2 genotype in children was nearly 1.6 times as frequent as the vacAs1 genotype (61.2 and 36.7% respectively). In adult patients vacAs2 genotype was detected 2.5 times less frequently than vacAs1 (27.6 and 70.7%, respectively). VacAm2 genotype was revealed in 71.4% (35/49) of children and 77.6% (45/58) of adults. IceA2 genotype was identified in 46.9% (23/49) of children and 44.8% (26/58) of adult patients, iceA1 gene - in 20.4% of children and 55.2% of adult patients. Conclusion. The strains with vacAs2m2 genotype are prevailing in children (42.9%) and determine low toxigenicity of H. pylori strains; vacAs1m2 genotype is predominant among adult patients (53.4%); high prevalence of cagA-negative strains of H. pylori was found both in children and adults (73.5 and 67.2%, respectively).


2016 ◽  
Vol 6 (11) ◽  
pp. 942-946
Author(s):  
Shiva Raj K.C. ◽  
A Lakhey ◽  
K Koirala ◽  
GL Amatya

Background: Dyspepsia is a prevalent complaint in general practice and gastrointestinal clinics. Helicobacter pylori have major causal relationship with gastro duodenal disease. The following study seeks to identify the prevalence of H. pylori based on histology and to correlate endoscopic findings with histopathology.Materials and Methods: This was a cross-sectional observational study conducted in GRP Polyclinic and Om Hospital and research centre from April 2015-September 2015. The upper gastrointestinal endoscopic findings were recorded and were correlated with histopathological findings. All the relevant data were collected and analysed using Statistical Package of Social Sciences version 16 for windows.  Results: Endoscopy finding was divided into reflux esophagitis, antral gastritis, duodenitis, duodenal ulcer, gastric ulcer, and gastric cancer. Duodenal ulcer and gastric ulcer was noted more frequently in males than in females (55.0% vs. 45.0% and 58.2% vs. 41.8%), respectively, P < 0.001).Chronic follicular gastritis was the most common in gastric ulcer (41.7%), whereas chronic persistent gastritis was common in non-ulcerative disease. Chronic active gastritis and chronic follicular gastritis were more common in ulcerative diseases, whereas chronic persistent gastritis was more common in gastritis and duodenitis (P < 0.001). The overall prevalence of H. pylori infection was 68.1% with male preponderance. Chronic active gastritis had highest prevalence of H. pylori (84.8%), followed by chronic follicular gastritis (84.1%) and chronic persistent gastritis (p value < 0.001.Conclusion: Rate of H. pylori infected patients with dyspepsia was high. Ulcerative lesions were more common in males than in females with higher rate of infection with H. Pylori.  Histological diagnosis of chronic active gastritis and chronic follicular gastritis was the most common pathologies in ulcerative lesions. 


2018 ◽  
Vol 16 ◽  
pp. 1721727X1875726
Author(s):  
Fang Xu ◽  
Cai-ling Mai ◽  
Qian Zhu

Helicobacter pylori infections have been one of the major factors associated with gastroduodenal ulcer. Toll-like receptors (TLRs) of human recognize mycobacterium-induced immune response and protect subjects from disease pathogenesis. Variants in TLR genes are believed to influence immune responses to H. pylori and clinical severity. TLR-9 polymorphisms have been associated with susceptibility to gastroduodenal ulcer in different populations. In this study, we investigate the role of common TLR-9 variants in susceptibility/resistance to the development of gastroduodenal ulcer in a Chinese cohort. The present hospital-based case–control study enrolled 580 patients with abdominal discomfort, and based on endoscopic investigation, the patients were categorized into (1) gastric ulcer (n = 154), (2) duodenal ulcer (n = 70), (3) gastric and duodenal ulcers (n = 25), (4) gastritis (n = 195), and (5) healthy stomach (n = 136). A total of 520 healthy controls from similar geographical areas were enrolled as controls. TLR-9 (C-1237T, C-1486T, and G+2848A) polymorphisms were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Plasma levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β in both healthy controls and patients were quantified by enzyme-linked immunosorbent assay (ELISA). Furthermore, messenger RNA (mRNA) expressions of TNF-α, IL-6, and IL-1β in biopsy tissues were quantified by real-time polymerase chain reaction (RT-PCR). The prevalence of TLR-9+2848 heterozygotes (CT) was significantly higher in gastroduodenal ulcer patients compared to healthy controls. Sub-categorization of patients revealed higher prevalence of heterozygotes of TLR-9 C+2848T and C-1486T polymorphisms in patients with gastric ulcer (GU), duodenal ulcer (DU), and those with both gastric and duodenal ulcers (GDU) when compared to controls. Patients displayed higher plasma cytokine levels than healthy controls. TLR-9 polymorphisms (C+2848T and C-1486T) correlated with altered cytokine expression in biopsy tissues and their plasma levels. In conclusion, TLR-9 (C+2848T and C-1486T) polymorphisms are associated with gastroduodenal ulcer and correlated with altered cytokine levels.


2005 ◽  
Vol 23 (16) ◽  
pp. 3768-3772 ◽  
Author(s):  
Ariela Noy ◽  
Joachim Yahalom ◽  
Leah Zaretsky ◽  
Ian Brett ◽  
Andrew D. Zelenetz

Purpose Gastric mucosa-associated lymphoid tissue (MALT) lymphoma is indolent and often associated with Helicobacter pylori bacterial infection. H pylori–independent MALT develops either in the absence of the bacteria or persists after bacterial eradication. We have previously demonstrated long-term pathologic remission after involved-field radiotherapy therapy (IFRT). We determined molecular remission status by clonotypic polymerase chain reaction (PCR). Patients and Methods Twenty-four consecutive patients with stage I to IIE gastric MALT lymphoma who obtained a pathologic remission after IFRT alone were evaluated. All had at least two follow-up endoscopic gastroduodenal biopsies at Memorial Sloan-Kettering Cancer Center. IFRT median dose was 30 Gy (range, 28.5 to 43.5 Gy). Post-treatment biopsies were subjected to semi-nested clonotypic PCR. Results All patients obtained a complete response based on routine immunohistochemical pathologic analysis of random post-treatment gastric biopsies. Median follow-up from completion of IFRT was 63 months (range, 19 to 117 months). Event-free survival was 96%; 23 of 34 patients remained in clinical and pathologic complete remission. Baseline DNA extraction yielded 17 clone-specific primer pairs. At the first follow-up test, 14 of 17 pairs were PCR positive. Eight remained persistently positive; and one was persistently negative. Others were intermittently positive. Conclusion Despite sustained biopsy-proven remissions for as long as 117 months after radiation, the vast majority of patients remain positive by clonotypic PCR. This suggests that the malignant clone is present but missing either an internal or external signal essential to the cancer phenotype. One possibility is that radiation eradicates the polyclonal H pylori–specific T cells eliminating critical local factors necessary for proliferation of the monoclonal B cells.


2021 ◽  
Vol 8 (8) ◽  
pp. 171-175
Author(s):  
Tara Rizvira Monica ◽  
Gontar Alamsyah Siregar ◽  
Taufik Sungkar

Mucosal damage in people with gastritis causes the production of VEGF. VEGF is a neoangiogenesis function to repair damaged tissue. Excess production can cause cancer risk. VEGF genotype polymorphisms are thought to affect the production of serum VEGF levels. The aim of this study was to determine the relationship between VEGF - 2578 C> A polymorphism and serum VEGF levels in H. pylori gastritis. Method: cross-sectional study was conducted at H. Adam Malik General Hospital and Network Hospital with 100 samples. Endoscopic examination was performed to assess the gastric mucosa and a tissue biopsy was performed. The urea breath test (UBT) test and the Campylobacter like organism (CLO) test to determine H. pylori infection. VEGF - 2578 C> A was checked by Polymerase Chain Reaction (PCR). The data will be analyzed by univariate and bivariate. Result: One hundred people with gastritis, of which 59 people were infected with H. pylori. In this study, H. pylori infection did not have a significant relationship with VEGF levels. VEGF - 2578 C> A polymorphisms also had no relationship to serum VEGF levels. Conclusion: There is no correlation between VEGF - 2578 C> A polymorphism with VEGF serum levels (p> 0.05). Keywords: VEGF polymorphisms, VEGF - 2578 CA, H. pylori, Gastritis.


2020 ◽  
Vol 15 (2) ◽  
Author(s):  
Tariq Elhashim ◽  
M. Imad Mustafa Mahmud ◽  
Nasser Amjad ◽  
Norra Harun ◽  
Imad M. Alani

Introduction: H. pylori BabA is an outer membrane protein that mediates bacterial adherence to the gastric epithelium, triggers several pathways during the course of infection, and thus contributes to the disease development. Considering the variability in the presence of BabA coding gene (babA2) among H. pylori clinical strains, the aim of this study was to assess the relationship between the genotype status of H. pylori babA2 and the severity of clinical and histopathological outcomes. Methods: Gastric mucosal biopsy specimens were collected from 30 CLO test-positive patients, 16 with gastritis and 14 with peptic ulcer disease. Polymerase chain reaction was carried out to detect the presence of H. pylori-specific glmM gene and BabA coding gene (babA2). Histopathological examination was performed to evaluate the severity of H. pylori-associated gastric disease according to the Updated Sydney Classification System. Results: The glmM and babA2 genes were present in 100% and 86.7% of the tested H. pylori strains, respectively. Although higher degrees of inflammatory activity and H. pylori density were noted in babA2-positive biopsy specimens, there was no statistically significant association between babA2 genotype status and the severity of gastric disease. Conclusion: The babA2 genotype status of H. pylori may not be considered as a sole marker for determining the infection outcomes.


1970 ◽  
Vol 2 (2) ◽  
pp. 6-10 ◽  
Author(s):  
A Sultana ◽  
SM Badruddoza ◽  
F Rahman

This study had been planned to see the histomorphological pattern of gastric mucosal biopsy, demonstrate the organism H .Pylori and correlate with endoscopic findings. The study was carried out in the department of the Pathology Rajshahi Medical College, Rajshahi, Bangladesh, during the period from January 2006 to December 2007. Endoscopic biopsy specimens were obtained from 105 cases of gastro duodenal lesions. According to endoscopic findings out of 105 cases 69(65.7%) had gastric carcinoma, 06 (5.71%) had gastric ulcer, 05 (4.76%) had duodenal ulcer, 05 (476%) had gastritis and 20 (19.04%) had normal mucosa, reported as non-ulcer dyspepsia. Of the 69 endoscopically gastric carcinoma 59 (85.50%) were diagnosed histologically as adenocarcinoma and 10 (14.50%) were diagnosed histologically as chronic gastritis in which H.Pylori was positive in 27.5% and 14.50% positive in chronic gastritis. Of 06 gastric ulcer 03 (50%) was diagnosed histologically as gastritis and 03 (50%) were diagnosed histologically as gastric carcinoma. H. Pylori was positive in cent percent of gastritis. Of 05 duodenal ulcer 03 (60%) were diagnosed histologically as gastritis and 02 (40%) were diagnosed histologically as intestinal metaplasia H. Pylori was positive in 66.6% of duodenal ulcer. Of 05 gastritis were diagnosed histologically as gastritis 60% were postive for H.Pylori. Of 20 NUD 18 (90%) were diagnosed histologically as gastritis, 01 (05%) was diagnosed histologically as ulcer and 01 (05%) was diagnosed histologically as normal mucosa, all these cases no H. Pylori was found. Key Words: Helicobacter Pylori; Gastroduodenal Lesion; Association DOI: http://dx.doi.org/10.3329/akmmcj.v2i2.8164 AKMMC J 2011; 2(2): 06-10


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