Treatment strategies and preventive methods for drug-resistant Helicobacter pylori infection

The infection and drug resistance rates of Helicobacter pylori(H.pylori)are high and must be prevented and treated by better strategies.Based on recent research advances in this field as well as the results from our team and those on traditional Chinese medicine,we review the causes of drug resistance,and prevention and treatment strategies for drug-resistant H.pylori infection,with an aim to make suggestions for the development of new drugs,such as establishment of new target identification and screening systems,modification of existing drug structures,use of new technologies,application of natural products,and using a commercial compound library.This article may provide reference for eradication of drug-resistant H.pylori.

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.

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.

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.

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.

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.

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 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

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:

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

Helicobacter pylori infection and respiratory diseases:a review

In the past few years,a variety of extradigestive disorders, including cardiovascular,skin,rheumatic and liver diseases, have been associated with Helicobacter pylori(H.pylori) infection.The activation of inflammatory mediators by H.pylori seems to be the pathogenetic mechanism underlying the observed associations.The present review summarizes the current literature,including our own studies,concerning the association between H.pyloriinfection and respiratory diseases. A small number of epidemiological and serologic,case- control studies suggest that H.pylori infection may be associated with the development of chronic bronchitis.A frequent coexistence of pulmonary tuberculosis and H.pylori infection has also been found.Moreover,recent studies have shown an increased H.pyloriseroprevalence in patients with bronchiectasis and in those with lung cancer.On the other hand,bronchial asthma seems not to be related with H.pylori infection. All associations between H.pylori infection and respiratory diseases are primarily based on case-control studies, concerning relatively small numbers of patients.Moreover, there is a lack of studies focused on the pathogenetic link between respiratory diseases and H.pylori infection. Therefore,we believe that larger studies should be undertaken to confirm the observed results and to clarify the underlying pathogenetic mechanisms.

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.

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 and oral pathology:Relationship with the gastric infection

Helicobacter pylori(H.pylori)has been found in the oral cavity and stomach,and its infection is one of the most frequent worldwide.We reviewed the literature and conducted a Topic Highlight,which identified studies reporting an association between H.pylori-infection in the oral cavity and H.pylori-positive stomach bacterium.This work was designed to determine whether H.pylori is the etiologic agent in periodontal disease,recurrent aphthous stomatitis(RAS),squamous cell carcinoma,burning and halitosis.Record selection focused on the highest quality studies and meta-analyses.We selected 48 articles reporting on the association between saliva and plaque and H.pylori-infection.In order to assess periodontal disease data,we included 12 clinical trials and 1 meta-analysis.We evaluated 13 published articles that addressed the potential association with RAS,and 6 with squamous cell carcinoma.Fourteen publications focused on our questions on burning and halitosis.There is a close relation between H.pylori infection in the oral cavity and the stomach.The mouth is the first extra-gastric reservoir.Regarding the role of H.pylori in the etiology of squamous cell carcinoma,no evidence is still available.

Can Helicobacter pylori infection influence human reproduction?

Helicobacter pylori (H. pylori) infection could be associated with extra-digestive diseases. Here, we report the evidences concerning the decrease in reproductive potential occurring in individuals infected by H. pylori, especially by strains expressing CagA. This infection is more prevalent in individuals with fertility disorders. Infected women have anti-H. pylori antibodies in cervical mucus and follicular fluid that may decrease sperm motility and cross react immunologically with spermatozoa, conceivably hampering the oocyte/sperm fusion. Infection by CagA positive organisms enhances the risk of preeclampsia, which is a main cause of foetus death. These findings are supported by the results of experimental infections of pregnant mice, which may cause reabsorption of a high number of foetuses and alter the balance between Th1 and Th2 cell response. Infected men have decreased sperm motility, viability and numbers of normally shaped sperm and augmented systemic levels of inflammatory cytokines, such as tumor necrosis factor-&#x003b1;, which may damage spermatozoa. In countries where parasitic infestation is endemic, detrimental effects of infection upon spermatozoa may not occur, because the immune response to parasites could determine a switch from a predominant Th1 type to Th2 type lymphocytes, with production of anti-inflammatory cytokines. In conclusion, the evidences gathered until now should be taken into consideration for future studies aiming to explore the possible role of H. pylori infection on human reproduction.

Is there an association between Helicobacter pylori infection and irritable bowel syndrome? A meta-analysis

BACKGROUND Irritable bowel syndrome(IBS)is a prevalent and debilitating gastrointestinal condition.Research has reported persistent,low-grade mucosal inflammation and significant overlaps between patients with IBS and those with dyspepsia,suggesting a possible pathogenic role of Helicobacter pylori(H.pylori)in IBS.This study therefore aimed to provide the first systematic review and meta-analysis on the association between H.pylori infection and IBS.AIM To investigate the association between H.pylori infection and IBS.METHODS Using the keywords“H.pylori OR Helicobacter OR Helicobacter pylori OR infection”AND“irritable bowel syndrome OR IBS”,a preliminary search of PubMed,Medline,Embase,Cochrane Database of Systematic Reviews,Web of Science,Google Scholar and WanFang databases yielded 2924 papers published in English between 1 January 1960 and 1 June 2018.Attempts were also made to search grey literature.RESULTS A total of 13 clinical studies were systematically reviewed and nine studies were included in the final meta-analysis.Random-effects meta-analysis found a slight increased likelihood of H.pylori infection in patients with IBS,albeit this was not statistically significant(pooled odds ratio 1.47,95%confidence interval:0.90-2.40,P=0.123).It must also be acknowledged that all of the available studies reported only crude odd ratios.H.pylori eradication therapy also does not appear to improve IBS symptoms.Although publication bias was not observed in the funnel plot,there was a high degree of heterogeneity amongst the studies included in the meta-analysis(I2=87.38%).CONCLUSION Overall,current evidence does not support an association between IBS and H.pylori infection.Further rigorous and detailed studies with larger sample sizes and after H.pylori eradication therapy are warranted.