Family-based Helicobacter pylori infection status and transmission pattern in central China,and its clinical implications for related disease prevention

BACKGROUND Helicobacter pylori(H.pylori)has characteristics of family cluster infection;however,its family-based infection status,related factors,and transmission pattern in central China,a high-risk area for H.pylori infection and gastric cancer,have not been evaluated.We investigated family-based H.pylori infection in healthy households to understand its infection status,related factors,and patterns of transmission for related disease prevention.AIM To investigate family-based H.pylori infection status,related factors,and patterns of transmission in healthy households for related disease prevention.METHODS Blood samples and survey questionnaires were collected from 282 families including 772 individuals.The recruited families were from 10 selected communities in the greater Zhengzhou area with different living standards,and the family members’general data,H.pylori infection status,related factors,and transmission pattern were analyzed.H.pylori infection was confirmed primarily by serum H.pylori antibody arrays;if patients previously underwent H.pylori eradication therapy,an additional 13C-urea breath test was performed to obtain their current infection status.Serum gastrin and pepsinogens(PGs)were also analyzed.RESULTS Among the 772 individuals examined,H.pylori infection rate was 54.27%.These infected individuals were from 246 families,accounting for 87.23%of all 282 families examined,and 34.55%of these families were infected by the same strains.In 27.24%of infected families,all members were infected,and 68.66%of them were infected with type I strains.Among the 244 families that included both husband and wife,spouse co-infection rate was 34.84%,and in only 17.21%of these spouses,none were infected.The infection rate increased with duration of marriage,but annual household income,history of smoking,history of alcohol consumption,dining location,presence of gastrointestinal symptoms,and family history of gastric disease or GC did not affect infection rates;however,individuals who had a higher education level showed lower infection rates.The levels of gastrin-17,PGI,and PGII were significantly higher,and PGI/II ratio was significantly lower in H.pylori-infected groups than in H.pylori-negative groups.CONCLUSION In our study sample from the general public of central China,H.pylori infection rate was 54.27%,but in 87.23%of healthy households,there was at least 1 H.pylori-infected person;in 27.24%of these infected families,all members were infected.Type I H.pylori was the dominant strain in this area.Individuals with a higher education level showed significantly lower infection rates;no other variables affected infection rates.

Is Helicobacter pylori infection protective against esophageal cancer?

Helicobacter pylori(H.pylori)infection affects a substantial proportion of the global population and causes various gastric disorders,including gastric cancer.Recent studies have found an inverse relationship between H.pylori infection and eso-phageal cancer(EC),suggesting a protective role against EC.This editorial focuses on the possible mechanisms underlying the role of H.pylori infection in EC and explores the role of gut microbiota in esophageal carcinogenesis and the prac-ticality of H.pylori eradication.EC has two major subtypes:Esophageal squamous cell carcinoma(ESCC)and esophageal adenocarcinoma(EAC),which have different etiologies and risk factors.Gut microbiota can contribute to EC via inflammation-induced carcinogenesis,immunomodulation,lactagenesis,and genotoxin production.H.pylori infection is said to be inversely related to EAC,protecting against EAC by inducing atrophic gastritis,altering serum ghrelin levels,and triggering cancer cell apoptosis.Though H.pylori infection has no significant association with ESCC,COX-2-1195 polymorphisms and endogenous nitrosamine production can impact the risk of ESCC in H.pylori-infected in-dividuals.There are concerns regarding a plausible increase in EC after H.pylori eradication treatments.However,H.pylori eradication is not associated with an increased risk of EC,making it safe from an EC perspective.

Association between central serous chorioretinopathy and Helicobacter pylori infection: a systematic review and Meta-analysis

AIM:To investigate the association between central serous chorioretinopathy(CSC)and Helicobacter pylori(Hp)by summarizing all available evidence.METHODS:The Scopus,Embase,EBSCO,PubMed,Web of Science,and Cochrane Library databases for all relevant studies published from inception to October 2022 were searched,and manually searched for relevant reference lists as a supplement.Studies investigating the association between CSC and Hp infection were included.Finally,8 case-control studies were included in the Meta-analysis after study selection.RESULTS:The results showed no significant correlation between Hp infection and CSC[odds ratio(OR)1.89,95%confidential interval(CI)0.58–6.15,I2=96%,P=0.29].After subgroup analysis based on the degree of development of the study(developing/developed countries),it was found that the results of the two subgroups were the same as the whole,and no significant difference between the two subgroups existed.Meta-regression showed that the effect of sample size on heterogeneity among studies was more prominent(P<0.01,adjusted R^(2)=89.72%),which can explain 89.72%of the sources of heterogeneity.CONCLUSION:This Meta-analysis reveals no significant correlation between Hp infection and CSC,which still warrants further well-designed extensive sample studies to reach a more reliable conclusion and promote a better understanding of the treatment of CSC.

Effect of acacetin on inhibition of apoptosis in Helicobacter pyloriinfected gastric epithelial cell line

BACKGROUND Helicobacter pylori(H.pylori)infection can cause extensive apoptosis of gastric epithelial cells,serving as a critical catalyst in the progression from chronic gastritis,gastrointestinal metaplasia,and atypical gastric hyperplasia to gastric carcinoma.Prompt eradication of H.pylori is paramount for ameliorating the pathophysiological conditions associated with chronic inflammation of the gastric mucosa and the primary prevention of gastric cancer.Acacetin,which has multifaceted pharmacological activities such as anti-cancer,anti-inflammatory,and antioxidative properties,has been extensively investigated across various domains.Nevertheless,the impact and underlying mechanisms of action of acacetin on H.pylori-infected gastric mucosal epithelial cells remain unclear.AIM To explore the defensive effects of acacetin on apoptosis in H.pylori-infected GES-1 cells and to investigate the underlying mechanisms.METHODS GES-1 cells were treated with H.pylori and acacetin in vitro.Cell viability was assessed using the CCK-8 assay,cell mortality rate via lactate dehydrogenase assay,alterations in cell migration and healing capacities through the wound healing assay,rates of apoptosis via flow cytometry and TUNEL staining,and expression levels of apoptosis-associated proteins through western blot analysis.RESULTS H.pylori infection led to decreased GES-1 cell viability,increased cell mortality,suppressed cell migration,increased rate of apoptosis,increased expressions of Bax and cle-caspase3,and decreased Bcl-2 expression.Conversely,acacetin treatment enhanced cell viability,mitigated apoptosis induced by H.pylori infection,and modulated the expression of apoptosis-regulatory proteins by upregulating Bcl-2 and downregulating Bax and cleaved caspase-3.CONCLUSION Acacetin significantly improved GES-1 cell viability and inhibited apoptosis in H.pylori-infected GES-1 cells,thereby exerting a protective effect on gastric mucosal epithelial cells.

Estimate the Prevalence of Helicobacter pylori Infection among Diabetes & Non-Diabetes Mellitus Patients and Its Correlation with Malignant Gastritis Patients Attending in Lower Shabelle Region (Somalia)

Background: Several conducted studies have reported a higher and more frequent Helicobacter pylori infection rate in type 2 diabetes mellitus (T2DM). The aim of this study was to estimation the prevalence of H. pylori and its association between H. pylori infection and T2DM. Materials and Methods: A sectional-cross study was conducted based on 200 patients studded with socioeconomic characteristics through a questionnaire & H. pylori was diagnosed by serum anti-H. pylori immunoglobulin G (IgG) and IgA. Furthermore, patients were investigated for fasting blood glucose (FBG) levels, glycosylated hemoglobin (HbA1c), serum cholesterol, and other biochemistry parameters. Results: The findings showed The prevalence of Hp positive infection was significantly higher in the total sample was 134 with (67%). While 66 out of 200 patients with (33%) was H. pylori negative infection. of H. pylori. Further, the mean values were statistically significant for diabetes with H. pylori infection for IgG > 300 titer and IgA > 250 titer, regarding, HbA1C (7.52 ± 0.41) (P Conclusions: The current study revealed that H. pylori prevalence infections were significantly higher in diabetic patients studied compared to non-diabetic patients. Furthermore, T2DM patients infected with H. pylori positive reported a higher prevalence rate of symptoms than H. pylori negative.

Potential Risk of Transmission of Escherichia coli and Salmonella spp. Infections by the Musca domestica Fly and the Periplaneta americana Cockroach in the City of Cotonou (South Benin)

Background: The occurrence of bacterial infections sometimes involves synanthropic flies and cockroaches, as mechanical vectors of pathogenic microorganisms. The aim of this study was to identify the different species of flies and cockroaches that cohabit with humans in the city of Cotonou and determine the contribution of Musca domestica and Periplaneta americana in the transmission of bacteria responsible for infections in humans. Methods: Capture sessions during the day for flies and at night for cockroaches were carried out in 4 arrondissements of the city of Cotonou. The insects collected were transported to the Center of Research Entomological of Cotonou for identification, then sent to the Section Hygiene of Water and Food for microbiological analysis, enumeration and testing for human pathogenic bacteria. Results: A total of 351 flies and 26 cockroaches were collected at the sites, including two synanthropic species belonging to two families each. Musca domestica and Periplaneta americana were the most abundant species found after identification in the city of Cotonou. Thermo-tolerant coliforms and Escherichia coli were found on all specimens at varying concentrations. Salmonella spp. bacteria were identified in the fly population from the Dantokpa dump. Conclusion: Flies and cockroaches can transmit microorganisms to humans. The presence of Salmonella spp. among the specimens revealed that infections frequently caused by contaminated food or water are also transmitted to humans by flies. The presence of these germs on flies and cockroaches represents a potential risk of mechanical transmission to humans. It is, therefore, essential to continue investigations in order to assess the species of bacteria propagated, improve control strategies against these troublesome insects and adopt better hygiene conditions for better living.

Helicobacter Pylori Infections in Peptic Ulcer Perforations: A Retrospective Analysis in Two Referral Hospitals in Douala, Cameroon

Background: Perforations are major complications of peptic ulcer disease and surgical emergencies with important mortality and morbidity. Helicobacter pylori (H. pylori) has been identified as one of the commonest factors associated with peptic ulcer disease. However, little is known about its implication in cases of perforations in Cameroon. We aimed to determine the frequency of Helicobacter pylori infections in cases of perforated peptic ulcers, describe clinical features and outcomes of these cases in Cameroon. Method: A hospital-based retrospective cross-sectional study was conducted through the review of patients’ records admitted for peptic ulcer perforations in Laquintinie and Douala General Hospitals over a period of 5 years (January 2014 - December 2018). We defined H. pylori infection as;positive result on tissue biopsy at time of surgery. We used SPSS version 23.0 to analyse data and set an alpha value at P = 0.05. Results: We reviewed 115 cases of peptic ulcer perforation, with a mean age of 40 years and sex ratio (M:F) of 5:1. All patients underwent emergency laparotomy, 48 (41%) cases had a biopsy report and the prevalence of H. pylori infection in these cases was 47.9 %. Smoking, alcohol consumption and Non-Steroidal Anti-inflammatory Drugs (NSAIDs) use, were not associated with peptic ulcer perforation. The morbidity was at 43.7% and mortality at 14%. Mortality was increasing with a higher Mannheim Peritonitis Index score (OR: 23.51, 95% CI: 4.197 - 143.003, P-value: 0.000). Conclusion: We observed a high prevalence of H. pylori infection in patients with peptic ulcer perforations. We recommend systematic H. pylori screening in cases of perforations and that larger studies should be carried out to evaluate the association of H. pylori infection with peptic ulcer perforation in Sub-Saharan Africa.

An epidemiologic study of Helicobacter pylori infection in three areas with high,medium or low incidence of gastric carcinoma

AIMS To study the relation of Helicobacter pylori (Hp) infection rate to the incidence of and mortality from gastric cancer. METHOD Hp infection rate of natural population in three areas was detected by measuring the specific IgG-antibody to Hp using indirect ELISA method. RESULTS Hp positive rate was 59.4%,55.9% and 34.5% in the areas with high,medium and low inci- dence of gastric carcinoma respectively. The differ- ences in incidence among the areas were significant (x^2 =25.029,P<0.05). In persons under 40 years of age,the Hp infection rate was the highest in high inci- dence area of gastric cancer. Hp infection rate was 50% in children under 5 years of age in the high inci- dence area. In the people under 40 years of age,the Hp infection rates showed no difference among the three areas. The average levels of anti-Hp IgG in high, medium and low incidence areas were 2.3±0.49, 2.04±0.47 and 1.84±0.46 respectively. Multivariate regression analysis showed that Hp infection is related to bad hygienic habit,low income,frequent use of an- tibiotics and mental depression. Single factor analysis showed that Hp infection may also be related to raising animals in home. CONCLUSION Gastric cancer is closely related to the incidence of Hp infection.

Helicobacter pylori infection

IS THERE ANYTHING NEW?Helicobacter pylori has been for many years aforgotten bacterium,since the first report on thisspiral organism dated from the 19th century.Asearly as in 1906,an association between a spiralorganism and gastric carcinoma was suggested.Doenges reported in 1938 that on autopsy not

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.

Furazolidone-based triple and quadruple eradication therapy for Helicobacter pylori infection

AIM: To evaluate the efficacy of furazolidone-based triple and quadruple therapy in eradicating Helicobacter pylori (H. pylori) in a multi-center randomized controlled trial.

Effect of Helicobacter pylori infection on gastric epithelial proliferation in progression from normal mucosa to gastric carcinoma

AIM To study the effect of Helicobacter pylori ( H. pylori ) infection on gastric epithelial proliferation in the progression from normal mucosa to gastric carcinoma. METHODS Gastric biopsy specimens from normal controls ( n =11), superficial gastritis ( n =32), atrophic gastritis with intestinal metaplasia ( n =83), dysplasia ( n =25) and gastric carcinoma ( n =10) were studied by immunohistochemical staining of proliferating cell nuclear antigen (PCNA). RESULTS The gastric epithelial proliferation, expressed as PCNA labeling index (LI)%, was progressively increased in successive stages from normal mucosa to gastric carcinoma regardless of H. pylori status. There was significant difference in PCNA LI% among all groups ( P <0 01). The analysis pursuing the effect of H. pylori infection on gastric epithelial proliferation in the progression from normal mucosa to gastric carcinoma showed that in superficial gastritis and mild atrophic gastritis groups, PCNA LI% in H. pylori positive patients were 13 14±1 6 and 19 68±2 22 respectively, significantly higher than 6 95±0 78 and 11 34±1 89 in H. pylori negative patients ( P <0 01); but there was no such difference in other groups ( P >0 05). CONCLUSION H. pylori infection causes increased gastric epithelial proliferation in the stages of superficial and mild atrophic gastritis and may play a part in triggering gastric carcinogenesis.

Study of T-lymphocyte subsets,nitric oxide,hexosamine and Helicobacter pylori infection in patients with chronic gastric diseases

Chronic gastritis ( CG ) and peptic ulcer ( PU ) are frequently-occurring diseases. It is now well recognized that Helicobacter pylori (Hp) is a major factor that leads to CG and PU[1-8] In order to study the relationship among T lymphocyte subsets, NO, Hexosamine and Hp infection in patients with chronic gastric diseases, the levelsof blood T lymphocyte subsets, plasma NO and hexosamine in gastric mucosa were measured respectively in 30 patients with CG and 32 patients of PU + CG.

Helicobacter pylori: the primary cause of duodenal ulceration or a secondary infection?

INTRODUCTIONIt is generally accepted that Helicobacter pylori ( H.pylori) infection has a role in duodenal ulceration .Eradicaton of H .pylori accelerates healing compared with placebo in the absence of control of gastric secretion and reduces ulcer recurrence .There is increasing evidence ,however ,that is may not be the primary cause of duodenal ulceration ,but that is may be a secondary factor in a nnmber of cases .This possibility is supported by four sets of observations : 1 Geographical distribution:

Strategies used by helicobacter pylori to establish persistent infection

Helicobacter pylori(H. pylori) is a Gram-negative and motile bacterium that colonizes the hostile microniche of the human stomach, then persists for the host's entire life, if not effectively treated. Clinically, H. pylori plays a causative role in the development of a wide spectrum of diseases including chronic active gastritis, peptic ulceration, gastric adenocarcinoma, and gastric mucosaassociated lymphoid tissue lymphoma. Due to the global distribution of H. pylori, it is no exaggeration to conclude that smart strategies are contributing to adaptation of the bacterium to its permanent host. Thirty-four years after the discovery of this bacterium, there are still many unanswered questions. For example, which strategies help the bacterium to survive in this inhospitable microniche? This question is slightly easier to answer if we presume the same clinical concept for both persistent infection and disease. Understanding the mechanisms governing H. pylori persistence will improve identification of the increased risk of diseases such as gastric cancer in patients infected with this bacterium. A well-defined and longterm equilibrium between the human host and H. pylori allows bacterial persistence in the gastric microniche; although this coexistence leads to a high risk of severe diseases such as gastric cancer. To escape the bactericidal activity of stomach acid, H. pylori secretes large amounts of surface-associated and cytosolic urease. The potential to avoid acidic conditions and immune evasion are discussed in order to explain the persistence of H. pylori colonization in the gastric mucosa, and data on bacterial genetic diversity are included. Information on the mechanisms related to H. pylori persistence can also provide the direction for future research concerning effective therapy and management of gastroduodenal disorders. The topics presented in the current review are important for elucidating the strategies used by H. pylori to help the bacterium persist in relation to the immune system and the many unfavorable features of living in the gastric microniche.

Helicobacter pylori infection and gastrointestina hormones:a review

INTRODUCTIONHelicobacter pylori(Hp)infection is closely relatedto gastrointestinal hormones and involves theformation of gastritis,gastric carcinoma and pepticulcer.Its pathogenesis relevant

Seroepidemiology of Helicobacter pylori infection among asymptomatic Chinese children

INTRODUCTIONIncreasing data has demonstrated that Helicobacterpylori(H.pylori),a spiral gram negativebacterium,colonized in human stomach,can causetype B gastritis,is strongly associated withgastric and duodenal ulceration,and has beenimplicated in the causation of gastric carcinomaand mucosa-associated lymphoid tissue(MALT)lymphomas.It has been reported that there

Simple animal model of Helicobacter pylori infection

Helicobacter pylori(H.pylori)has become accepted as a human pathogen for the development of gastritis and gastroduodenal ulcer.To develop a simple rat model of chronic H.pylori infection,male Sprague-Dawley rats were pretreated with streptomycin suspended in tap water(5 mg/mL)for 3 d.The rats were inoculated by gavage at 1 mL/rat with H.pylori suspension(5×108-5×1010 CFU/mL)twice daily at an interval of 4 h for three consecutive days.Two weeks after inoculation,rats were sacrificed and the stomachs were removed.Antral biopsies were performed for urease test and the stomachs were taken for histopathology.Successful H.pylori inoculation was defined as a positive urease test and histopathology.We reported a 69.8%-83.0%success rate for H.pylori infection using the urease test,and hematoxylin and eosin staining confirmed the results.Histopathological analysis detected bacteria along the mucous lining of the surface epithelium and crypt lumen and demonstrated mild to moderate gastric inflammation in successfully inoculated rats.We developed a simple rat model of chronic H.pylori infection for research into gastric microcirculatory changes and therapy with plant products.

Association between TNF-a and IL-1β genotypes vs Helicobacter pylori infection in Indonesia

AIM:To investigate the correlation between the Helicobacter pylori(H.pylori)infection and host genetic background of healthy populations in Indonesia.METHODS:In March 2007,epidemiological studies were undertaken on the general population of a city in Indonesia(Mataram,Lombok).The participants included 107 men and 187 women,whose ages ranged from6 to 74 years old,with an average age of 34.0(±14.4)(±SD).The H.pylori of subject by UBT method determination,and through the polymerase chain reaction with confronting two-pair primers(PCR-CTPP)method parsing the single nucleotide polymorphism of interleukin(IL)-8,IL-4,IL-1β,CD14,tumor necrosis factor(TNF-a)and tyrosine-protein phosphates non-receptor type 11(PTPN11)genotypes.The experimental data were analyzed by the statistical software SAS.RESULTS:The H.pylori infection rates in the healthy Indonesian population studied were 8.4%for men and12.8%for women;no obvious differences were noted for H.pylori infection rates by sex or age.TC genotypes of IL-4,TC and CC genotypes of TNF-a,and GA genotypes of PTPN11,were higher in frequency.Both CC and TC genotype of TNF-a T-1031C loci featured higher expressions in the healthy Indonesian population Indonesia studied of(OR=1.99;95%CI:0.67-5.89)and(OR=1.66;95%CI:0.73-3.76),respectively.C allele of IL-1βT-31C gene locus was at a higher risk(OR=1.11;95%CI:0.70-1.73)of H.pylori infection,but no statistical significance was found in our study.CONCLUSION:We reveal that the association between the TNF-a and IL-1βgenotypes may be the susceptibility of H.pylori in the studied population.

Helicobacter pylori infection and gastric carcinoma:Not all the strains and patients are alike

Gastric carcinoma(GC) develops in only 1%-3% of Helicobacter pylori(H. pylori) infected people. The role in GC formation of the bacterial genotypes, gene polymorphisms and host's factors may therefore be important. The risk of GC is enhanced when individuals are infected by strains expressing the oncoprotein CagA, in particular if CagA has a high number of repeats containing the EPIYA sequence in its C'-terminal variable region or particular amino acid sequences flank the EPIYA motifs. H. pylori infection triggers an inflammatory response characterised by an increased secretion of some chemokines by immunocytes and colonised gastric epithelial cells; these molecules are especially constituted by proteins composing the interleukin-1beta(IL-1β) group and tumour necrosis factor-alpha(TNF-α). Polymorphisms in the promoter regions of genes encoding these molecules, could account for high concentrations of IL-1β and TNF-α in the gastric mucosa, which may cause hypochlorhydria and eventually GC. Inconsistent results have been attained with other haplotypes of inflammatory and anti-inflammatory cytokines. Genomic mechanisms of GC development are mainly based on chromosomal or microsatellite instability(MSI) and deregulation of signalling transduction pathways. H. pylori infection may induce DNA instability and breaks of double-strand DNA in gastric mucocytes. Different H. pylori strains seem to differently increase the risk of cancer development run by the host. Certain H. pylori genotypes(such as the cagA positive) induce high degrees of chronic inflammation and determine an increase of mutagenesis rate, oxidative-stress, mismatch repair mechanisms, down-regulation of base excision and genetic instability, as well as generation of reactive oxygen species that modulate apoptosis; these phenomena may end to trigger or concur to GC development.