Positive Helicobacter Pylori Strains Research Articles

Antibiotic-Resistant Strains of Helicobacter pylori in 50 Antibiotic Treatment-Naive Children in Northeast Poland Diagnosed by Gastric or Duodenal Biopsy Between February 2019 and May 2022.

BACKGROUND In recent years, an increasing prevalence of Helicobacter pylori resistance to antibiotics has been observed. The aim of this study was to assess antibiotic resistance of Helicobacter pylori in previously untreated children from northeast Poland. MATERIAL AND METHODS Inclusion criteria comprised suspicion of Helicobacter pylori infection based on the presence of Helicobacter pylori antigen in the stool and/or characteristic macroscopic lesions seen on esophagogastroduodenoscopy. Samples of the gastric and/or duodenal mucosa were collected from 82 children with a median age of 13 years (range 3-17) during esophagogastroduodenoscopy between February 2019 and May 2022. The material was cultured, and positive Helicobacter pylori strains were tested for drug resistance to amoxicillin, metronidazole, and clarithromycin using the quantitative antibiotic concentration gradient stripe method E-test. RESULTS Based on biopsy culture, Helicobacter pylori infection was confirmed in 50 (61%) children. Helicobacter pylori resistance was most common to clarithromycin (n=19; 38%), followed by metronidazole (n=15; 30%), and the least frequent to amoxicillin (n=13; 26%). The resistance to 1 antibiotic was found in 14 children (28%). Double-drug resistance was noted in 3 children (6%) and triple drug resistance in 9 children (18%). In the whole group, 24 children (48%) were susceptible to all 3 antibiotics. CONCLUSIONS In this study, conducted for the first time in treatment-naïve children in northeast Poland, we found a high proportion of Helicobacter pylori strains resistant to at least 1 antibiotic. Our results may help in the appropriate choice of antibiotics for treatment of Helicobacter pylori in our region.

Evaluating the relationship between Helicobacter pylori infection and carotid intima-media thickness a cross sectional study

IntroductionHelicobacter pylori is a gram-negative spiral bacterium that is frequently found in the human stomach. Significant association has been reported between Cytotoxin associated gene A (CagA)- positive Helicobacter pylori strains and coronary heart disease. The aim of the present study is to investigate the carotid intima-media thickness as an indicator of atherosclerosis in people with Helicobacter pylori infection. MethodsThis study was done on patients who underwent upper GI endoscopy and biopsy, and after obtaining conscious consent underwent ultrasound of the right and left carotid arteries for measuring carotid intima-media thickness (CIMT) and blood tests. ResultsIn this study, 90 patients who underwent upper GI endoscopy were examined in three groups: negative H. pylori negative, positive cagA and negative cagA. The right, left and average of CIMT in cagA-positive group were significantly higher than the other two groups (p < 0.05). Howerver, the average of CIMT was not significantly different between men and women. Also, the hsCRP average level in positive cagA group was significantly higher than other groups (p < 0.05). ConclusionOur findings suggest that there is an increase in CIMT values in patients with H. pylori infection, especially in cases of positive cagA. The positive cagA group showed significantly higher levels of hs-CRP, as a marker of elevated inflammatory response. Therefore, H. pylori infection, especially cagA-positive strains and its associated systemic inflammatory response can be considered as a contributing factor in atherosclerosis and cardiovascular disease.

Helicobacter Pylori Infection: Association with Hashimoto’s Thyroiditis

Autoimmune thyroid diseases (ATDS) are multifactorial conditions that result from genetic predisposition in combination with environmental risk factors. Helicobacter Pylori (HP) infection as an environmental risk factor has been proposed to initiate the antigenic components of the thyroid cell membrane and may play a leading role in the onset of the auto immune diseases such as Hashimoto's thyroiditis (HT). 1.1. The Aim: To investigate the association between H.P infection and HT and the prevalence of cag. A positive strains H.P in the patients. 1.2. Methods:The study include 40 female patients with Hashimoto's thyroiditis as a case group and 30 healthy female as control group. HP antigen in stool samples using unamplified enzyme immunoassay and Cag. Ainserum samples using an enzyme linked immunoassay method (ELISA). Anti-thyroid peroxidase antibodies (anti TPO) and thyroid function tests thyroid stimulating hormone (TSH) and thyroxine (T4) were determined. 1.3. Results:There is statistically significant association between H P and HT (Odd ratio = 8.1, 95% confidence interval: 3-30.1, p<0.001). Also statistically significant association between presence of Cag-A positive strains of HP and HT (odd ratio=5.3, p=0.001). To establish the significant correlation between HP and HT further and more specialized studies are needed. 1.4. Conclusion:There was a significant association between Hashimoto's thyroiditis and H.P infection and significant prevalence of cag. A positive strain of H.P positive patients and HT

Cytotoxin-associated gene antigen-positive strains of Helicobacter pylori and recurring acute coronary syndromes.

Cytotoxin-associated gene antigen (CagA)-positive strains of Helicobacter pylori have previously been associated with acute coronary syndromes. However, the role of CagA-positive strains of Helicobacter pylori in recurring cardiac events after ST-segment elevation myocardial infarction (STEMI) has not yet been assessed. We enrolled 181 consecutive patients (155 men, mean age 64±13 years) presenting with STEMI. In all patients, serum levels of IgG anti-CagA were assessed. Levels of IgG anti-hepatitis A virus were also evaluated in all patients in order to exclude the presence of a bystander activation of the immune system. Finally, a previous history of acute coronary syndrome and the rate of major adverse cardiovascular events as a composite of cardiovascular death, recurring myocardial infarction and target lesion revascularisation within 2 years follow-up were evaluated. Anti-CagA IgG seropositive patients presented more frequently with a previous history of acute coronary syndrome compared with seronegative patients (28.3% vs. 14%, P=0.019). Interestingly, no differences were observed between anti-CagA IgG seropositive and anti-CagA IgG seronegative patients concerning the prevalence of anti-hepatitis A virus IgG seropositivity (20% vs. 21.4%, P=0.48). At 2-year follow-up, 40 patients experienced major adverse cardiovascular events. The major adverse cardiovascular event rate was higher in anti-CagA IgG seropositive compared with seronegative patients (hazard ratio 2.25, 95% confidence interval 1.34-2.95, P=0.013), which was confirmed at Cox multivariate analysis (hazard ratio 2.33, 95% confidence interval 1.30-3.14, P=0.009). CagA-positive strains of Helicobacter pylori seem to be involved in the pathogenesis of recurring acute coronary syndromes, and seropositivity for anti-CagA IgG predicts prognosis after STEMI, possibly due to the increased risk of recurring cardiac events.

Role of Helicobacter pylori infection in pathogenesis of atherosclerosis.

Though a century old hypothesis, infection as a cause for atherosclerosis is still a debatable issue. Epidemiological and clinical studies had shown a possible association but inhomogeneity in the study population and study methods along with potential confounders have yielded conflicting results. Infection triggers a chronic inflammatory state which along with other mechanisms such as dyslipidemia, hyper-homocysteinemia, hypercoagulability, impaired glucose metabolism and endothelial dysfunction, contribute in pathogenesis of atherosclerosis. Studies have shown a positive relations between Cytotoxic associated gene-A positive strains of Helicobacter pylori and vascular diseases such as coronary artery disease and stroke. Infection mediated genetic modulation is a new emerging theory in this regard. Further large scale studies on infection and atherosclerosis focusing on multiple pathogenetic mechanisms may help in refining our knowledge in this aspect.

Insights into the Role of Helicobacter pylori Infection in Preeclampsia: From the Bench to the Bedside.

Preeclampsia (PE) is defined as a hypertensive and coagulative disorder affecting about 2–8% of all pregnancies and is one of the main causes of maternal and fetal morbidity and mortality. Despite the great amount of studies run in this field, little is known about the precise pathogenic mechanisms behind PE. While endothelial and trophoblast dysfunctions, exaggerated inflammatory response, and hypercoagulative state have been shown to play a key role in the occurrence of PE, the primary trigger is still unknown. One of the hypotheses is that some infectious agents may represent a trigger for PE onset. Consistently, higher seroprevalence of Helicobacter pylori (HP) infection, a Gram-negative bacterium with a specific tropism for human gastric mucosa, has been shown in women with PE. Even tighter association has been found between PE and infection with cytotoxin-associated gene-A (CagA)-positive strains of HP. Recent in vitro studies have shown that anti-CagA antibodies cross-react with human trophoblast cells and determine a functional impairment in terms of cell invasiveness, thus, providing the first pathogenic model of HP infection-mediated placental damage. Since in the early process of implantation and placental development, trophoblast invasion of maternal decidua is a crucial step, the proposed autoimmune mechanism induced by HP infection, negatively interfering with the fetal side of the early developing placenta, may represent a mechanism explaining the higher seropositivity for HP infection among PE women. However, the contribution of HP infection to the pathogenesis of PE or to the worsening of its clinical presentation need to be further investigated as well as the possible impact of pre-pregnancy screening and eradication of HP infection on the incidence of the syndrome.

Interaction of omeprazole and Helicobacter pylori-induced nuclear factor-κB activation and mediators in gastric epithelial cells

BackgroundOmeprazole (OMP), a proton pump inhibitor, is a highly effective drug for the management of acid-related disorders. Infections resulting from cytotoxin antigen A (CagA) positive Helicobacter pylori strains have been associated with higher grades of gastric mucosal inflammation. Nuclear factor (NF)-κB activation has been reported to participate in H. pylori-induced gastritis in humans. The complex interaction of OMP on the H. pylori and NF-κB related molecular mechanisms within the gastric mucosa remains unclear. In the present study, we investigated OMP, specifically its effects on NF-κB activation, and COX-2, IL-6, and IL-8 production in gastric cells (Kato-III cells) treated with CagA positive (CagA+) and negative (CagA–) H. pylori strains. MethodsKato-III cells were stimulated with H. pylori water extracts (HPE) containing ATCC 43504 (CagA+) and ATCC 51932 (CagA–) strains. NF-κB activation, inhibitory IκB expression and phosphorylation, and cyclooxygenase (COX)-2, interleukin (IL)-6, and IL-8 expression were assessed in the absence and presence of OMP. ResultsBoth CagA+ and CagA– HPE induced NF-κB activation, whereas OMP suppressed NF-κB activation in the CagA– strain. HPE demonstrated a similar effect on IκB protein expression in the absence and presence of OMP. OMP alone decreased IκB phosphorylation without promoting NF-κB and IκB expression. Additionally, both CagA+ and CagA– HPE induced COX-2 expression, but no significant effect on IL-6 and IL-8. However, OMP downregulated the transcription of COX-2, IL-6, and IL-8 in CagA– HPE treated cells. ConclusionUsing the Kato-III cells model, H. pylori induces NF-κB activation in a CagA-independent manner. Both CagA+ HPE and CagA– HPE induced COX-2 gene expression, but not for IL-6 and IL-8 expression. However, OMP suppressed NF-κB activation via a downregulation of IκB phosphorylation in CagA– HPE treated condition. OMP also suppressed CagA–H. pylori induced-transcription of proinflammatory COX-2, IL-6, and IL-8. OMP may provide different effects on CagA+ and CagA–H. pylori infection conditions.

Autoimmune thyroid diseases andHelicobacter pylori: The correlation is present only in Graves's disease

To investigate the correlation between autoimmune thyroid diseases (ATDs) and the prevalence of Cag-A positive strains of Helicobacter pylori (H. pylori) in stool samples. Authors investigated 112 consecutive Caucasian patients (48 females and 4 males with Graves' disease and 54 females and 6 males with Hashimoto's thyroiditis HT), at their first diagnosis of ATDs. Authors tested for H. pylori in stool samples using an amplified enzyme immunoassay and Cag-A in serum samples using an enzyme-linked immunoassay method (ELISA). The results were analyzed using the two-sided Fisher's exact test and the respective odds ratio (OR) was calculated. A marked correlation was found between the presence of H. pylori (P ≤ 0.0001, OR 6.3) and, in particular, Cag-A positive strains (P ≤ 0.005, OR 5.3) in Graves' disease, but not in Hashimoto's thyroiditis, where authors found only a correlation with Cag-A strains (P ≤ 0.005, OR 8.73) but not when H. pylori was present. The marked correlation between H. pylori and Cag-A, found in ATDs, could be dependent on the different expression of adhesion molecules in the gastric mucosa.

High correlation of babA 2 -positive strains of Helicobacter pylori with the presence of gastric cancer

Helicobacter pylori (H. pylori) is a Gram-negative bacterium that is well known in the involvement of chronic inflammation in the gastric mucosa of the human stomach. Several studies have investigated the possible role of H. pylori presence in different gastroduodenal disorders with conflicting results. This study aimed to further investigate such a field. Helicobacter pylori strains were cultured from 160 patients (mean age of 42 years; range 15-75; 90 were male, and 70 were female) [40 gastric cancer (GC), 55 duodenal ulcer (DU) and 65 non-ulcer dyspepsia (NUD)]. In this study, allelic variants of iceA 1, iceA 2 and babA 2 were identified by polymerase chain reaction. The overall prevalence of babA 2 gene was 40.6% (65/160). The prevalence of babA 2 gene was 95% with gastric cancer, 18.1% with duodenal ulcer and 26.1% with non ulcer dyspepsia, respectively. The prevalence of babA 2 in GC patients was significantly higher as compared to either NUD or UD patients (P = 0.0004), while no statistical significance was found between the latter two patient groups. Our study finds that babA 2 and iceA 1 genes are more prevalent in GC compared to either NUD or DU patients in Iran.

Influence of CagA-positive Helicobacter pylori strains on atherosclerotic carotid disease

Citotoxin-associated gene-A (CagA)-positive Helicobacter pylori strains have been associated with occurrence and destabilization of coronary atherosclerotic plaques. However, data on the relationship between CagA-positive H. pylori infection and carotid artery instability are lacking. Thus, the role of CagA antigen in patients with symptomatic and asymptomatic carotid atherosclerotic plaques was investigated. A total of 64 patients with advanced carotid artery stenosis, including 33 patients with symptomatic and 31 patients with asymptomatic internal carotid artery stenosis, verified by duplex ultrasound, all undergoing carotid endarterectomy, were studied. The control group consisted of 65 subjects without a history or presence of vascular diseases. Serology for H. pylori and CagA antigen was assessed in all participants. Specimens of atherosclerotic plaques obtained from all patients during carotid endarterectomy were analyzed immunohistochemically using anti-CagA monoclonal antibodies. The ultrasonographic plaque characteristics were also estimated. CagA antibody titers were significantly higher in symptomatic patients (8.8; range, 5.8-32.7) compared to asymptomatic patients (4.7; range, 2.1-8.8; P = 0.005) and the control group (5.0; range 2.2-7.9; P < 0.001). There was significant difference in echolucency (≥ 25% soft material) between the symptomatic and asymptomatic groups (P = 0.034) by ultrasonographic evaluation. Positive immunoreactivity between monoclonal CagA antibodies and antigens within atherosclerotic specimens was significantly higher among symptomatic patients compared to asymptomatic patients (97.0 vs. 74.2%; P = 0.009). H. pylori may play a role in the pathogenesis of the atherosclerotic process due to autoimmune mechanisms and even contribute to destabilization of carotid atherosclerotic plaques.

Coronary atherosclerotic burden in patients with infection by CagA-positive strains of Helicobacter pylori

Cytotoxic associated gene-A (CagA)-positive strains of Helicobacter pylori emerged as a possible atherosclerotic stimulus. Nevertheless, whether CagA-positivity is associated with more extensive or severe atherosclerotic coronary burden has never been studied. Forty consecutive patients with coronary artery disease (CAD) and twenty consecutive patients with normal coronary arteries undergoing coronary angiography were enrolled. All patients underwent evaluation of classical atherogenic risk factors and assessment of anti-urease B and anti-CagA antibodies titer. Either the severity of coronary stenosis (stenosis score) or the extent of coronary atherosclerosis (extent score) was evaluated in CAD patients. The anti-CagA antibody titer was significantly higher in patients with CAD as compared with normal coronary arteries patients [85 (10-108.75) vs. 47.3 (17-64) RU/ml, P=0.02], whereas there were no differences in anti-urease B titer between the two groups. A significant correlation was found between anti-CagA antibody titer and extent score (R=0.35, P=0.03), whereas stenosis score was similar (R=0.25, P=0.11). On the contrary, no significant correlation was found between anti-urease B antibody titer and either extent or stenosis score. Moreover, CagA-positive patients had a more extensive CAD (P=0.029) when compared with CagA-negative patients. Interestingly, whereas serum glucose, LDL levels, anti-urease B, and anti-CagA antibodies were predictors of extent score at univariate analysis, at multivariate analysis anti-CagA antibody titer only was an independent predictor of the extent of coronary atherosclerosis (B=0.051, standard error of B=0.042, P=0.04). These results support the association between CagA-positive H. pylori infection and coronary atherosclerotic burden. Further studies are needed to better elucidate the mechanism by which CagA-positive strains may promote atherosclerosis.

Helicobacter pylori virulence and the diversity of gastric cancer in Asia

Infection with cagPAI positive strains of Helicobacter pylori is recognized as being associated with an increased risk of gastric cancer. This article reviews the current knowledge on the structures and pathological functions of cagPAI and the CagA protein, focusing especially on the molecular mechanism through which CagA may be involved in gastric carcinogenesis. The possible link between the geographical distribution of cagPAI and cagA variations and gastric cancer diversity in Asia is also discussed.

Abdominal aortic aneurysm and infection with CagA positive strains of Helicobacter pylori

The aim of the present study was to investigate whether virulent CagA positive Helicobacter pylori strains are those preferentially related to abdominal aortic aneurysm (AAA) rupture. Several microorganisms have been linked to aneurysm development. Chronic Chlamydophila pneumoniae infection has been suggested as a possible contributing factor for the development and expansion of AAA. Previous studies have shown increased risk of carotid atherosclerosis and coronary heart disease in subjects harbouring CagA positive strains of H. pylori. The relevance of CagA positive H. pylori involved in the processes underlying aneurysmal development, expansion, and rupture is unknown. In a case-control study, 119 patients with AAA and 36 matched controls were prospectively investigated with H. pylori serology. Patients with ruptured AAA have similar levels of IgG antibodies against H. pylori to patients with electively operated AAA, small AAA, and controls. In conclusion, this study fails to demonstrate a connection between H. pylori CagA seropositivity and abdominal aortic aneurysm rupture.

Virulent strains of Helicobacter pylori and vascular diseases: A meta-analysis

Cytotoxin-associated gene A (CagA)-positive strains of Helicobacter pylori are an etiological factor for peptic ulcer and gastric cancer. Studies on the role of these virulent strains in vascular diseases yield conflicting results. We searched the MEDLINE database for relevant studies. Meta-analysis was performed using the random effects method. We found 10 retrospective case-control studies (with 1527 case patients and 1661 control subjects) and 3 prospective cohort studies (with 701 case patients and 1439 control subjects) on CagA status and ischemic heart disease and 4 retrospective case-control studies (with 513 case patients and 590 control subjects) on CagA status and cerebral ischemia. In the case-control studies, an association of ischemic heart disease with CagA-positive strains (OR 1.87, 95% CI 1.46-2.40) but no significant association with CagA-negative strains (OR 1.15, 95% CI 0.83-1.60) has been found; in the 3 prospective studies, association with ischemic heart disease was weaker but still significant (OR 1.26, 95% CI 1.05-1.51). In the 4 case-control studies, CagA-positive strains were significantly associated with cerebral ischemia (OR 2.43, 95% CI 1.89-3.13), again with no association for CagA-negative strains. We found a small but significant association between vascular diseases and virulent CagA-positive strains of H. pylori. The lack of association with CagA-negative strains further supports the hypothesis of an independent relationship between virulent strains of H. pylori and vascular diseases. The magnitude of the association with cerebral ischemia needs to be confirmed by prospective studies.

Gastrin and gastric epithelial cell proliferation in subjects infected with CagA positive helicobacter pylori strains

Gastrin and gastric epithelial cell proliferation in subjects infected with CagA positive helicobacter pylori strains

Topographical localisation of cagA positive and cagA negative Helicobacter pylori strains in the gastric mucosa; an in situ hybridisation study

Background: The cagA gene is a marker for the presence of the cag pathogenicity island, and the presence of cagA positive strains of Helicobacter pylori can identify individuals with a...

CagA Positive Helicobacter Pylori Strains Are Associated with Increased Risk of Peptic Ulcer Bleeding Among NSAID Users. A Multicenter Case-Control Study

CagA Positive Helicobacter Pylori Strains Are Associated with Increased Risk of Peptic Ulcer Bleeding Among NSAID Users. A Multicenter Case-Control Study

Cytotoxin-associated gene-A--positive Helicobacter pylori strains are associated with atherosclerotic stroke.

It is uncertain whether Helicobacter pylori is associated with ischemic syndromes and whether this association is mediated by the induction of atherosclerosis. In this study, we tested the hypothesis that atherosclerotic stroke shows a selective association with virulent H pylori strains. The seroprevalence of infection by H pylori and by strains bearing the cytotoxin-associated gene-A (CagA), a strong virulence factor, was assessed by ELISA in 138 patients with large-vessel stroke (group A), in 61 patients with cardioembolic stroke (group B), and in 151 healthy control subjects. The 3 groups had a similar socioeconomic status. Serum levels of C-reactive protein were also measured by ELISA. The prevalence of infection was 71% in group A, 63.9% in group B, and 70.2% in the control group (P=NS), whereas the prevalence of CagA-positive strains was higher in group A than in group B (42.8% versus 19.7%, respectively; odds ratio 3.04, 95% CI 1.43 to 6.49; P<0.001) and higher in group A than in the control group (42.8% versus 17.9%, respectively; odds ratio 4.3, 95% CI 2.12 to 8.64; P<0.001), after adjusting for main cardiovascular risk factors and social class. A trend toward a difference in C-reactive protein was observed between CagA-positive (2.00+/-3.43 [mean+/-SD] mg/dL) and CagA-negative (1.31+/-1.72 [mean+/-SD] mg/dL) patients (P=0.072, Mann-Whitney U test). The association between H pylori and acute cerebrovascular disease seems to be due to a higher prevalence of more virulent H pylori strains in patients with atherosclerotic stroke.

Gastric permeability is not increased in children colonized by CagA-positive strains of Helicobacter pylori

Background. Sucrose permeability has been used as a marker to detect gastric lesions in children. As CagA status of Helicobacter pylori is an important factor in determining the evolution of the gastric lesion, CagA-positive strains being more frequently associated with severe mucosal lesions, the aim of this study was to determine the prevalence of CagA-positive strains in Helicobacter pylori-colonized children and to evaluate whether the sucrose permeability test might discriminate between colonization by CagA-positive or negative strains. Patients and methods. A series of 38 children (11.1 ±3.6 years] who required upper endoscopy for diagnostic purposes were included in the study. Endoscopy was carried out after the sucrose permeability test, and gastric biopsies were obtained for histologic examination, Helicobacter pylori detection by Giemsa staining and CLO-test, and determination of CagA status of the colonizing Helicobacter pylori strains by polymerase chain reaction. Results. Helicobacter pylori was detected in 26 subjects (68.4%) and of these, 16 (61.5%) were colonized by CagA-positive strains. The intensity of the histologic findings was significantly associated with the presence of Helicobacter pylori and with CagA status of the infecting strains ( χ 2=21.2, p=0.0017). However, no significant difference in the urinary excretion of sucrose between children not colonized and children with CagA-negative or positive strains was observed (0.027% (0.012-0.035%); 0.027% (0.016-0.047%) and 0.026% [0.016-0.038], median [range], respectively; Kruskal-Wallis analysis of variance F=0.75, p=O.69). Conclusions. These results indicate that in Chile, about 60% of the Helicobacter pylori infected children are colonized by CagA-positive strains, in association with more intense lesions of the gastric mucosa, but that gastric permeability to sucrose does not discriminate between colonization by CagA-negative and positive strains of Helicobacter pylori.

Risk for developing gastric carcinoma in patients colonized by cagA positive Helicobacter pylori strains

Risk for developing gastric carcinoma in patients colonized by cagA positive Helicobacter pylori strains