cagA Gene Research Articles

CagA and vacA allelic combination of Helicobacter pylori in gastroduodenal disorders

BackgroundAllelic variation of the virulence genes, vacA and cagA, as the most important virulence associated genes play an important role in the pathogenesis of severe gastrointestinal disease. ObjectiveThe aim of the present study was to identify the diversity of the virulence genes in patients with Gastric Cancer (GC), who were referred to the gastro-endoscopy unit of Imam Khomeini Hospital, Ahvaz Jundishapur University of medical science, Ahvaz, Iran. MethodsGastric biopsy specimens from 301 patients suspected to gastrointestinal disorders, were analyzed for H. pylori using molecular and phenotypical methods (culture, and biochemical test (catalase, oxidase and urease tests)). ResultsAmong 201 PCR positive for H. pylori, using histopathological methods, 22 (10.9%) patients had GC. Presence of vacA gene in our H. pylori strains was 100% (201/201), while the most virulent vacA s1 allele was detected in 82.6% isolates, and the mid region vacA m1 was found in 39.8% isolates. The vacA s1/m1 genotype was the most virulent allelic combination in GC and Peptic Ulcer Disease (PUD) in 68.2% and 50%, respectively. The cagA gene was detected in 66.7% isolates. Among the cagA positive isolates, EPIYA-ABC motif was the most common motif in the GC (66.7%), PUD (55.6%) and Erosive Gastroduodenitis (EG) samples (55.2%), while EPIYA-ABCC was the most common motif (58.7%) in the Non-Ulcer Dyspepsia (NUD) samples. The vacA s1m1/cagA+ combination was detected in GC (73.3%) and PUD (51.9%), while vacA s1m2/cagA+ presented in the NUD and EG samples in 77.8% and 62.1%, respectively. ConclusionIn this work, Western type (EPIYA-ABC and ABCC motifs) cagA, vacA s1m1 combinations have been demonstrated as the dominant genotype in the tested Ahvazian H. Pylori strains. Also the participation of cagA gene and vacA s1m1 genotype in development and severity of gastric disorder was well evident. Therefore, infection with H. pylori strain containing the cagA gene or the vacA s1m1 genotypes could be associated with increased risk of GC. This is the first study in our area that reports the high incidence and diversity of allelic combination of cagA and vacA genes in gastroduodenitis patients.

HELICOBACTER PYLORI INFECTION AND IMMUNE PROFILE OF PATIENTS WITH DIFFERENT GASTRODUODENAL DISEASES.

The association between infection with Helicobacter pylori and different gastroduodenal diseases is related to bacterial, host and environmental factors. Studies have demonstrated an association between the genetic diversity of H. pylori, especially in the vacA and cagA genes, and the development of digestive diseases such as peptic ulcer and gastric cancer. In addition, the nature of the host inflammatory response may explain these different manifestations of infection caused by this microorganism. In this respect, host factors that regulate the immune and inflammatory responses involving the functional interaction of H. pylori infection with different components of the immune system, particularly T cells, in gastroduodenal diseases still need further investigation. To characterize the immune response, including immunity induced by infection with H. pylori, especially virulent strains (vacA alleles and cagA gene), by analyzing the cytokine profile and T-cell population present in gastroduodenal diseases in a Brazilian population. In a prospective study, gastric biopsies were collected from 554 patients with different gastroduodenal diseases for histological analysis and for the determination of bacterial genotype and cytokine production (IL-4, IL-10, IFN-γ and IL-12) by ELISA. The predominant genotype of the H. pylori strains isolated from the patients studied was s1m1cagA+, which was more common among patients with gastric ulcer, duodenal ulcer and gastric cancer. A significant association was observed between the s1m1cagA+ genotype and a higher degree of inflammation, higher neutrophil activity and the development of intestinal metaplasia. The gastric concentrations of IFN-γ and IL-12 were significantly higher in patients infected with H. pylori than in uninfected individuals. Higher levels of these cytokines were detected in patients with gastric ulcer and cancer, while the levels of IL-4 and IL-10 in the gastric mucosa were lower in these patients. In addition, IFN-γ and IL-12 concentrations in gastric biopsies were higher in patients infected with the virulent s1m1cagA+ genotype. In contrast, IL-4 and IL-10 levels were higher in tissue infected with s2m2cagA in gastric biopsies. Our study shows that the interaction between the type of infectious strain and the Th1 immune response can influence and perpetuate gastric inflammation, and thus contributes to the development of the different clinical manifestations of H. pylori infection.

Association of oral Helicobacter pylori with gastric complications

AimThis study was aimed to identify the presence of Helicobacter pylori (H. pylori) genes in oral mucosa and find out their relationship between oral H. pylori infection and gastric complications. MethodsThis study is a case control study consists of 567 subjects with periodontal infection (278 gastric complication cases and 289 controls normal gastric intestinal mucosa) with age range of 20–80 years. Oral health status was recorded by calculating oral hygiene index (OHI), probing depths (PD) and clinical attachment loss (CAL). Each participant provided gastric biopsy and plaque samples which were subjected to H. pylori detection. Polymerase chain reaction (PCR) with different primers specifically β globulin, 16SrRNA, babA, cagA, ureA, ureC and vacA gene was performed which were then analyzed using gel electrophoresis. ResultsNo significant differences (χ2 = 11.873, p value > 0.05) were observed between oral H. pylori and gastric infections/complications. However, H. pylori increase the risk of developing gastro-esophageal reflux grade II (OR = 1.458, 95%CI = 0.659–3.226), normal upper GIT mucosa with lax esophageal sphincters (OR = 1.215, 95%CI = 0.285–5.181) and duodenal ulcer/duodenitis (OR = 2.187, 95%CI = 0.225–21.278). This study also showed a significant increased risk of gastritis with babA gene. ConclusionOral pathogenic H. pylori genes may enhance the severity of the gastric infection.

Association of H.pylori cagA Gene with Duodenal Ulcer & Gastric Carcinoma in Bangladeshi Patients

Background: Prolong infection with Helicobacter pylori may lead to chronic inflammation of gastroduodenal mucosa which in turns develops into severe diseases like peptic ulcer and gastric carcinoma. Bacterial virulence factor Cytotoxin Associated gene (cagA) is found to be responsible for developing such severe diseases in different countries. So this study was conducted to assess the relationship between occurrence of several gastroduodenal diseases and the presence of H. pylori cagA gene in Bangladeshi patients. Methods: Endoscopic gastroduodenal biopsy sample of 113 dyspeptic patients from different districts of Bangladesh were studied. H. pylori infection was detected by Rapid urease test, PCR of ureC gene and histological staining (Geimsa). Gastroduodenal disease was diagnosed by histopathological examination and cagA gene was detected by PCR. Result: H. pylori infection was identified among 48% (54/113) patients. Fifty seven percent of H. pylori infected patients were found to be cagA gene positive. cagA gene is significantly associated with Duodenal ulcer (p= .024) and Gastric carcimoma (p < .001). However, a further larger study is required to confirm this finding.

Usefulness of rapid urease test samples for molecular analysis of clarithromycin resistance in Helicobacter pylori

Helicobacter pylori is a gastric pathogen that is widely recognized as a causative agent of gastric disease. Its eradication is variable, mainly due to increased resistance to clarithromycin. Our objective was: to evaluate (i) if the biopsy specimen used for the rapid urease test is a useful sample to detect resistance to clarithromycin by PCR-RFLP and (ii) the distribution of A2142G and A2143G point mutations in the 23S rRNA gene, in relation to virulence factors in our region. Gastric specimens were collected from adult dyspeptic patients (n=141) and H. pylori was investigated by the rapid urease test, histopathological analysis and PCR for the hsp60 gene. Clarithromycin resistance was detected by PCR-RFLP in 62 H. pylori (+) paired biopsy specimens submitted to molecular analysis and the rapid urease test. H. pylori virulence factors were analyzed by multiplex PCR using specific primers for the cagA, vacA and babA2 genes. Thirteen out of 62 strains (20.9%) were resistant to clarithromycin: 6/13 (46.2%) harbored the A2143G mutation whereas 7/13 (53.8%) carried the A2142G point mutation. vacA m1s1 was the most frequent genotype among the resistant strains. In conclusion, the biopsy specimens used for the rapid urease test were suitable samples for clarithromycin resistance detection in patients infected with H. pylori, which became especially useful in cases where the number or size of the biopsies is limited. In addition, this is the first report of a molecular analysis for clarithromycin resistance performed directly from gastric biopsies in our region.

The clinical value of the polymerase chain reaction technique in detection of pediatric helicobacter pylori infection

Objective To investigate the clinical value of the polymerase chain reaction (PCR) technique in detection of pediatric helicobacter pylori(HP) infection. Methods A total of 130 children with different digestive tract symptoms received esophagogastroduodenoscopy, and 120 children between 3 and 17 years old were enrolled.The gastric antrum mucosa was taken under the gastroscope for 2 blocks, and the gastric juice was absorbed as the specimen.One block of gastric antrum mucosa was examined histopathologically, and the other block of gastric antrum mucosa and gastric juice were examined by PCR.We used the primers UreC, HP-16s, CSTP to detect HP, and then used the primers Cag750 and Cag595 to detect CagA. Results A total of 28 cases (23.33%) of upper gastrointestinal ulcer were detected by gastroscopy, and HP was detected by histopathological method in 26 cases (21.67%), and 41 cases (34.17%) were detected by PCR method.The detection rate of HP by PCR was significantly higher than that of HP in pathological method (χ2=4.659, P=0.031). By pathological examination of HP, 14 cases (50%) and 12 cases (13.04%) with peptic ulcers and no peptic ulcers were detectd, and the difference in detection rate was statistically significant(χ2=17.275, P<0.001). Samples of children with peptic ulcers and no peptic ulcers were detected in 16 cases(57.14%) and 25 cases (27.17%) by PCR, and the difference in detection rate was statistically significant (χ2=8.572, P=0.003). The CagA were detected in 7 cases of peptic ulcers and 7 cases of non peptic ulcers by PCR, and the difference in detection rate was statistically significant (25.00% vs 7.61%, χ2=6.300, P=0.012). Conclusion The PCR method could quickly and sensitively detect the HP and its CagA gene, and the detection of gastric mucosa and gastric juice by PCR could improve the detection rate of HP.A combination of PCR and pathological method is suggested as the detection method for children′s HP infection. Key words: Children; Helicobacter pylori; Histopathology examination; Polymerase chain reaction; CagA,

Serum TNF-α levels and Helicobacter pylori cagA and vacA genes

Helicobacter pylori is associated with higher virulence. TNF-α has an important role in host defense against H. pylori infection. The aim of this study was to investigate the relationship between TNF-α serum levels with cagA and vacA genes in H. pylori infection. This was a cross-sectional study involving 80 patients that consecutively admitted to endoscopy unit. Diagnosis of H. pylori infection was based on rapid urease test. Serum samples werecollected to determine circulating TNF-α level. Polymerase chain reaction was done to examine H. pylori vacA and cagA genes. Data analysis was carriedout using SPSS version 22 with 95%CI and p<0.05 was considered statistically significant. About 45 (56.3%) patients infected with Helicobacter pylori. There were 33 (73.3%) patients with H. pylori cagA positive. Serum TNF-α levels in patients with the H. pylori positive were significantly higher compared to H. pylori negative. Serum level of TNF-α was significantly higher in cagA positive than negative. Subjects with H. pylori cagA gene positive were more likely to have ahigher level of serum TNF-α than H. pylori cagA gene negative.

Primary antibiotic resistance and its relationship with cagA and vacA genes in Helicobacter pylori isolates from Algerian patients.

The epidemiology of Helicobacter pylori resistance to antibiotics is poorly documented in Africa and especially in Algeria. The aim of our study was to determine the antibiotic resistance rates, as well as its possible relationship with VacA and CagA virulence markers of isolates from Algerian patients. One hundred and fifty one H. pylori isolate were obtained between 2012 and 2015 from 200 patients with upper abdominal pain. Antimicrobial susceptibility testing was performed for amoxicillin, clarithromycin, metronidazole, ciprofloxacin, rifampicin and tetracycline. Molecular identification of H. pylori and the detection of vacA and cagA genes were performed using specific primers. We found that H. pylori was present in 83.5% of collected biopsies, 54.9% of the samples were cagA positive, 49.67% were vacA s1m1, 18.30% were vacA s1m2 and 25.49% were vacA s2m2. Isolates were characterized by no resistance to amoxicillin (0%), tetracycline (0%), rifampicin (0%), a high rate of resistance to metronidazole (61.1%) and a lower rate of resistance to clarithromycin (22.8%) and ciprofloxacin (16.8%). No statically significant relationship was found between vagA and cagA genotypes and antibiotic resistance results (p > 0.5) except for the metronidazole, which had relation with the presence of cagA genotype (p = 0.001).

Helicobacter pylori in a poultry slaughterhouse: Prevalence, genotyping and antibiotic resistance pattern.

Although Helicobacter pylori (H. pylori) is a highly significant pathogen, its source remains unclear. Many people consume chicken daily as a source of animal protein worldwide; thus, hygienic methods of supplying chickens for consumption are critical for public health. Therefore, our study examined the distribution of the glmM (ureC), babA2, vacA and cagA virulence genes in H. pylori strains in chicken meat and giblets (gizzards and livers) and the resistance of the strains to various antibiotics. Ninety chicken meat, gizzard and liver samples were obtained from a semi-automatic abattoir in Sadat City, Egypt, and were cultured and preliminarily analyzed using biochemical tests. The presence of the ureC, babA2, vacA and cagA genotypes was tested for in samples positive for H. pylori by multiplex polymerase chain reaction (Multiplex-PCR). The resistance of H. pylori to various antimicrobial drugs was tested using the disc diffusion method. In total, 7 of the 90 chicken samples were positive for H. pylori (7.78%); in 3/7 (42.85%) samples, the bacteria were found in the chicken liver, while the bacteria were found in the meat in 2/7 (28.57%) and in the gizzard in 2/7 (28.57%) samples. The total prevalence of both the ureC and babA2 genes in the isolated H. pylori strains was 100%, while the prevalence of the vacA and cagA genes was 57.1% and 42.9%, respectively. The resistance of H. pylori to the antibiotics utilized in our study was 100% for streptomycin; 85.7% for amoxicillin and penicillin; 71.4% for oxytetracycline, nalidixic acid and ampicillin; 57.1% for sulfamethoxazole and erythromycin; and 42.9% for neomycin, chloramphenicol and norfloxacin. In conclusion, the chicken meat and giblets were tainted by H. pylori, with a higher occurrence of the ureC, babA2, vacA and cagA genotypes. Future investigations should investigate the resistance of H. pylori to various antimicrobial agents in Egypt.

Transfection of the Helicobacter pylori CagA gene alters MUC5AC expression in human gastric cancer cells.

Helicobacter pylori, the primary causative agent of stomach cancer, is known to affect gastric mucin expression. However, the underlying molecular mechanisms mediating this H. pylori-dependent effect remain unknown. In the present study, the effect of exogenous expression of the H. pylori virulence factor, CagA, on mucin 5AC oligomeric muscus/gel-forming (MUC5AC) expression was investigated using an in vitro model of the gastric mucosa. AGS cells were either untreated or transfected by a vector control (pCDNA3.1) or heterologous DNA, which induced CagA overexpression (pCDNA3.1-CagA). The expression and functionality of MUC5AC was analyzed using the reverse transcription-quantitative polymerase chain reaction and immunofluorescence assays. The expression of H. pylori-CagA in AGS cells was able to significantly upregulate MUC5AC expression compared to the vector control. In addition, immunofluorescence assays were able to validate increased MUC5AC expression following exogenous expression of H. pylori-CagA. The results of the present study revealed that the H. pylori-derived virulence factor CagA was able to increase the expression of MUC5AC. As this mucin constitutes an important ecological niche for H. pylori, this response may be involved in H. pylori colonization of the stomach.

Helicobacter pylori infection increases sirt2 gene expression in gastric epithelial cells of gastritis patients

BackgroundHelicobacter pylori Infection causes some clinical features of the human stomach such as gastritis, duodenal ulcer, and gastric cancer. It has been shown that Helicobacter pylori infection increases proinflammatory cytokine gene expressions in Gastric Epithelial Cells by activation of NF-kB signaling. Sirt1 and sirt2 as deacetylases play a certain role in the progress of inflammation in arthritis and lung infection by impacting the NF-kB. AimsSirt1 and sirt2 gene expressions in Gastric Epithelial cells of gastritis patients were surveyed with and without Helicobacter pylori infection and rate of prevalence of cagA and hopQ genes in Helicobacter pylori strains were investigated. Methods25 biopsy samples of gastritis patients with Helicobacter pylori infection and 25 biopsy samples of gastritis patients without Helicobacter pylori infection were collected from Tohid Hospital in the city of Sanandaj throughout the year 2016. CDNA was made from total RNA extracted from biopsy samples (Qiagen® Kit). Sirt1 and sirt2 gene expressions were determined using the Corbett machine (Rotor-Gene 6000 Software). CagA and hopQ genes of Helicobacter pylori strains were determined by PCR using specific primers. ResultsThe sirt2 gene expression was increased in Gastric Epithelial Cells of gastritis patients with Helicobacter pylori infection. No significant relationship was found between sirt1 and sirt2 gene expressions as well as cagA and hopQ as Helicobacter pylori virulence genes. ConclusionsThis study shows the Helicobacter pylori infection duo to sirt2 gene up-expression. There is not a statistically significance relationship between cagA and hopQ Helicobacter pylori genotypes and sirt2 gene up-expression in Gastric Epithelial Cells of gastritis patients.

The Prevalence of Helicobacter pylori in Estonian Bariatric Surgery Patients.

Helicobacter pylori (Hp) is one of the most important human pathogens that can cause duodenal and gastric ulcers, gastritis and stomach cancer. Hp infection is considered to be a cause of limiting access to bariatric surgery. The aim of this study was to determine the prevalence of Hp in patients with obesity going into bariatric surgery and to reveal the relationship between Hp and clinical data. The study group was formed of 68 preoperative bariatric surgery patients (body mass index (BMI) 44.7 ± 4.8). Gastric biopsies (antrum and corpus) were used for histological and molecular (caqA and glmM genes) examinations. The PCR method revealed Hp infection in 64.7% of obese patients that is higher in comparison with histological analysis (55.9%). The prevalence of cagA and glmM genes in antrum mucosa was 45.6% and 47.0% while in the corpus it was 41.2% and 38.3%, respectively. The coincidence of both cagA and glmM virulence genes in the antrum and corpus mucosa was 33.8% and 22.1%, respectively. Either of the genes was found in 58.8% of antrum and 57.3% of corpus mucosa. Presence of caqA and glmM genes was in association with active and atrophic chronic gastritis. In conclusion, our study demonstrated that two thirds of morbidly obese patients undergoing bariatric surgery are infected with Hp and have a high prevalence of cagA and glmM virulence genes that points out the necessity for diagnostics and treatment of this infection before surgery.

Detection of DNA H.pylori and distribution of CagA genotype in cancerous and precancerous tissue

Helicobacter pylori (H. pylori) has been recognized as the causative agent of chronic gastric inflammation, which can progress further to a variety of diseases such as peptic ulcer and adenocarcinoma. The major bacterial virulence markers of H. pylori, the cytotoxin-associated gene (CagA), may play a role in determining the clinical outcome of Helicobacter infections. Aim of this study to investigate the presence of H.pylori DNA within gastric epithelial cells in patients with H.pylori infection and to determine the prevalence of CagA among patients with cancerous and precancerous lesion. Methods: A total of 92 gastric biopsy samples, 25 H.pylori negative and 67 H.pylori positive patients. H.pylori DNA in gastric epithelial cells and CagA gene of H. pylori was assessed by using the in situ hybridization test. Results: In H. pylori positive group, the positive rates of H.pylori DNA in the gastric epithelial cells were progressively increased in chronic superficial gastritis, precancerous changes and gastric cancer groups(P&gt;0.01); The detection of CagA positive H. pylori was significantly higher in patients with gastric cancer compared to those with chronic superficial gastritis and atrophic gastritis(P&lt;0.01). Conclusion: The pathological progression from chronic superficial gastritis, precancerous changes to gastric cancer is associated with higher positive rates of H.pylori DNA presence in the gastric epithelial cells, and there was a significant increase in CagA-positive H.pylori among patients with gastric cancer

VacA s1m1 genotype and cagA EPIYA-ABC pattern are predominant among Helicobacter pylori strains isolated from Mexican patients with chronic gastritis.

PurposeVirulent genotypes of Helicobacter pylori vacA s1m1/cagA+/babA2+ have been associated with severe gastric diseases. VacA, CagA and BabA are polymorphic proteins, and their association with the disease is allele-dependent. The aims of this work were: (i) to determine the prevalence of H. pylori by type of chronic gastritis; (ii) to describe the frequency of cagA, babA2 and vacA genotypes in strains from patients with different types of chronic gastritis; (iii) to characterize the variable region of cagA alleles.MethodologyA total of 164 patients with chronic gastritis were studied. Altogether, 50 H. pylori strains were isolated, and the status of cagA, babA2 and vacA genotypes was examined by PCR. cagA EPIYA segment identification was performed using PCR and sequencing of cagA fragments of six randomly selected strains.Results/Key findingsThe overall prevalence of H. pylori was 30.5 %. Eighty percent of the isolated strains were vacA s1m1, and the cagA and babA2 genes were detected in 74 and 32 % of the strains, respectively. The most frequent genotypes were vacA s1m1/cagA+/babA2- and vacA s1m1/cagA+/babA2+, with 40 % (20/50) and 28 % (14/50), respectively. In cagA+, the most frequent EPIYA motif was -ABC (78.4 %), and EPIYA-ABCC and -ABCCC motifs were found in 10.8 % of the strains. A modified EPIYT-B motif was found in 66.6 % of the sequenced strains.ConclusionH. pylori strains carrying vacA s1m1, cagA+ and babA2- genotypes were the most prevalent in patients with chronic gastritis from the south of Mexico. In the cagA+ strains, the EPIYA-ABC motif was the most common.

Helicobacter pylori cagA gene Polymorphism in Patients with Gastroduodenal Diseases

Helicobacter pylori is a genetically diverse bacterial pathogen and its CagA gene is a major virulence factor that plays an important role in gastroduodenal pathologies. The biological function of cagA depends on tyrosine phosphorylation within the EPIYA (Glutamate-Proline-Isoleucine-Tyrosine-Alanine) motifs at the C-terminal region of the protein. This region may undergo polymorphism to give different types of EPIYA motifs. EPIYA motif diversity may provide a useful tool for prediction of H. pylori pathogenic activity and accurate determination of number and type of cagA EPIYA motifs could identify the virulent H. pylori. The aim of this study was to detect H. pylori cagA gene and its polymorphism in endoscopic gastroduodenal biopsy specimen from patients with gastroduodenal diseases in Bangladesh. This cross sectional study was carried out in the Department of Microbiology &amp; Immunology, Bangabandhu Sheikh Mujib Medical University and Center for Advanced Research in Sciences, University of Dhaka during the period from March 2014 to February 2015. Gastric biopsies were collected from 78 patients with gastritis, duodenal ulcer, gastric ulcer and gastric carcinoma. H. pylori was identified by rapid urease test and ureC gene PCR. Presence of cagA gene and number and pattern of cagA EPIYA motif were determined by PCR. DNA sequencing was carried out to confirm the PCR detection method of cagA EPIYA motif and to analyse their peptide sequence. Among 31(39.7%) H. pylori positive cases, 19 (61.3%) were cagA gene positive in 11(55%) gastritis, 4(66.7%) duodenal ulcer, 2(66.7%) gastric ulcer and 2(100%) gastric carcinoma. A significant association was found between cagA gene and duodenal ulcer (p=˂0.05). EPIYA motif of all H. pylori cagA positive cases showed Western type cagA EPIYA ABC. No East Asian EPIYA ABD motif was found. Majority of gastroduodenal cases (57.9%) had 3 copies of EPIYA (ABC type), 26.3% had 4 copies (ABCC type) while remaining 10.5% had AC and 5.2% AB type EPIYA motif. EPIYA ABC was found in 75% of duodenal ulcer followed by 54.5% of gastritis and 50% of both gastric ulcer and gastric carcinoma patients. EPIYA ABCC motif was found in 50% of gastric ulcer and gastric carcinoma patients. Most of the EPIYA motif was EPIYA ABC and some were ABCC which has the risk of developing gastric carcinoma.

Prevalence of Helicobacter pylori cagA and iceA Genes and Their Association with Gastrointestinal Diseases.

H. pylori infection causes peptic ulcer, chronic gastritis, mucosa-associated lymphoid tissue lymphoma, and gastric carcinoma. It has several virulence factors such as cytotoxin-associated gene A(cagA) and the induced by contact with epithelium antigen (iceA). We aimed to explore the relationship between cagA and iceA of H. pylori and gastrointestinal diseases. One hundred and eighteen patients who attended Gastrointestinal Endoscopy Unit at Zagazig University Hospitals, Egypt, were included in this study. Two gastric biopsies were collected and evaluated by rapid urease test (RUT) and PCR. cagA and iceA genes were amplified by PCR. We found that 54 patients (45.76%) were positive by both RUT and PCR. cagA and iceA genes were present in 57.4% and 46.29% of the studied patients, respectively. cagA was the most prevalent gene in gastritis (33.3%) and peptic ulcer (68.7%). iceA1/iceA2 positive genes were the most prevalent in gastric cancer (75%). iceA1 gene was present in 38.7% of cagA positive cases, but iceA2 gene was present in 45.2% of cagA positive cases. iceA1/iceA2 positive genes were present in 29% of cagA positive cases. In conclusion, cagA and iceA genes could be used as markers for severe gastrointestinal diseases. iceA gene was strongly related to cagA gene.

CagA and VacA genes of Helicobacter pylori and their clinical relevance.

: Helicobacter pylori is associated with the development of a variety of gastroduodenal diseases which varies with ethnicity and the type of strains that infect the population. This study aims to evaluate the prevalence of H. pylori cagA and vacA genotypes in our region and to determine their relationship to the severity of the lesions that they cause. : This study was an observational cross-sectional study. DNA was extracted from 165 gastric biopsies from patients evaluated for dyspepsia. PCR was used to detect cagA and vacA (s1, s2, m1, m2) genes of H. pylori. Statistical analysis of associations was performed between endoscopy findings and virulence genes. Pearson Chi-square test and Fischer's exact test. The prevalence of H. pylori infection was 37% and the dominant genotypes was vacA s1 cagA-positive strain (54.1%) in this study. The vacAs1 subtype was found in all patients with peptic ulcer disease (PUD). The entire normal study group had VacA s2 variant only. This clearly shows that vacA s1 is a significant virulence marker and patients harboring s1 strains are more prone to develop ulcers (P = 0.007). There was a significant association of cagA with s1 strain rather than s2. Variation in VacA m genotype did not seem to have any association with disease status. There was a statistically significant association between the presence of cagA gene and PUD rather than the nonulcer dyspepsia (P = 0.027). The predominant genotype in our population was cagA positive vacA s1, which was found to be significantly associated with patients with gastric diseases, especially PUD. VacA s1 can serve as a single best virulence marker of the disease manifestation.

Analysis of Helicobacter pylori Genotypes Amongst Jordanians’ Dental Plaque Samples

BackgroundHelicobacter pylori (H. pylori) infection has been associated with gastritis, gastric ulcer, mucosa-associated lymphoid tissue lymphoma and gastric cancer. The prevalence of H. pylori virulence genes have been studied in different populations and from different sources of samples but their prevalence has not been studied in dental plaque in Jordanian people; therefore, the aim of this study was to determine the genotypes of H. pylori isolated from dental plaque samples.MethodsDental plaque samples were collected from 60 Jordanian volunteers. The genotypes of H. pylori virulence genes including the cytotoxin-associated gene A (cagA) and the vacuolating toxin (vacA) were determined using polymerase chain reaction (PCR).ResultsThe cagA gene was detected in 14 (23.3%) samples, while vacA was detected in all volunteers enrolled in this study (100%). The most prevalent vacA alleles were m2 and s1 in 54 (90%) and 55 (91.7%) of volunteers, respectively. Compared to the other combinations including the most virulent vacA genotype s1/m1 which was detected in 11 (18.2%) of volunteers, the most prevalent vacA allelic combinations were s1/m2 and s2/m2 in 56 (93.3%) and 27 (45%) of volunteers, respectively.ConclusionsThese results indicate a significant carriage of virulent H. pylori strains among Jordanian people in their dental plaques, which increases the possible transmission of these strains among them. In addition, the studying of the genotypic pattern of H. pylori virulence genes in the dental plaque could represent an essential tool for infection prevention and predicting the severity and prognosis of H. pylori gastric infection.

Prevalence and Diversity of Cag (PAI) in Helicobacter pylori: Study on Gastric Ulcer

Background: Frequency of H. Pylori in northern part of Iran within normal population is about 90% which is high, particular marker in order to diagnose patients with higher risk of peptic ulcer disease progression would be helpful for clinical practice. The purpose of this study was to evaluate the variable locus of CagA gene in virulence form. Methods: For this aim 200 types of biopsy infected and positive urease test and 20 samples of healthy people biopsies in order for control were provided. After DNA purification, the variety of locus in CagA gene was confirmed by glmM, SSA and CagV primers. Results: The results showed that 142 typical were positive for CagA. CagV primer used to variety fixed. The CagV gene exposed a special genetic variety in the 800 bp, 825 bp, 850 bp, 900 bp areas. Conclusions: The result of study on this locus suggested that variation of CagV could be consider as a paradigm in intensity and distribution of the gastric ulcer disease and key marker to prevent progression or inhibition of the progress in gastrointestinal disease.

Determination of Helicobacter pylori virulence-associated genes in duodenal ulcer and gastric biopsies

Background:Helicobacter pylori (H. pylori or Hp) has been strongly associated with the peptic ulcer diseases, chronic gastritis, ulcers, and gastric cancer. Genes associated with pathogenicity have been designated for H. pylori, and some of them appear to be related to more severe clinical consequences of the infection. The present study was conducted to determine cagA, vacA, cagE, iceA1, oipA, and iceA2 genes in H. pylori strains isolated from gastroduodenal patients, who referred to Shariati hospital in Tehran, Iran. Methods: Gastric biopsy specimens were collected during endoscopy from patients, who referred to the Shariati hospital in Tehran, Iran during January and November 2015. After isolation of H. pylori from the biopsy culture, genomic DNA was extracted and subsequently used to identify H. pylori and virulence genes using specific primers. Results: The isolation rate of H. pylori strains was 65.7% (169/257). The frequency of cagA, vacA, cagE, iceA1, oipA, and iceA2 was 143 (% 84.6), 169 (100%), 131 (77.5%), 97 (57.3%), 89 (52.6%), and 72 (42.6%), respectively. Conclusion: In this study, a significant difference was observed between investigated genes and strains isolated from PUD and GC patients (p<0.05).