cagA Strains Research Articles

Expression of CDX2, CK20 and CK7 in the epithelium of the gastric mucosa in schoolchildren with CagA H. pylori-associated gastritis

Aim. To study the association of protein expression CDX2, CK20, CK7 in the epithelium of the gastric mucosa in schoolchildren with CagA H. pylori-associated gastritis. Material and methods. Gastroscopy was performed with the collection of biopsy material from the mucous membrane of the antrum and body of the stomach in 89 schoolchildren (7-17 years old) with gastroenterological complaints. The morphological method confirmed the diagnosis of gastritis and determined the presence of H. pylori. Gastric biopsies were examined immunohistochemically to identify the proteins CDX2, CK20, CK7 in the epithelium. Blood was also collected to determine the CagA strain of H. pylori using enzyme immunoassay. Results. In schoolchildren infected with CagA H. pylori, higher expression of CK7 was found in both parts of the stomach (in the body (p = 0.044), in the antrum (p = 0.014)) compared to uninfected children. Changes in the expression of CDX2 and CK20 in children infected with H. pylori CagA have not been established. CDX2 protein was detected more often among schoolchildren aged 12-17 years with H. pylori infection than in children without H. pylori (p = 0.062) and in children with CagA H. pylori (p = 0.017). In the group of younger children with CagA H. pylori, there were higher levels of CK7 expression in the epithelium of the antrum of the stomach, compared with uninfected children (p = 0.033). They also had higher CK7 in the body than in CagA H. pylori-associated gastritis in children of the older age group (p = 0.001). Boys with CagA H. pylori had the highest expression of CK7 in the gastric body, which was higher than in uninfected boys (p = 0.021). Conclusion. Thus, in children, the features of the association of CDX2, CK20, CK7 with CagA H. pylori-associated gastritis have been established, including depending on the age and gender of the child.

Characterization of Helicobacter pylori iceA and babA2 virulence genes in dyspeptic patients at a teaching hospital in Ghana.

Helicobacter pylori (H. pylori) infection is endemic in Africa. It is a major aetiological factor in the development of peptic ulcer disease and distal gastric cancers. Existing data shows that clinical outcomes are dependent on the virulence of the infecting strain, host´s susceptibility, and environmental factors. In Ghana, a previous study showed that the majority of symptomatic individuals harboured cagA and vacA virulent strains. The main objective of this study was to characterize and assess the significance of other virulence factors, specifically iceA and babA2 in Ghana. H. pylori iceA and babA2 genes were investigated in dyspeptic patients at the Korle Bu Teaching Hospital (KBTH), Accra, Ghana. The study employed a cross-sectional design consecutively recruiting patients with upper gastrointestinal symptoms for endoscopy. Nucleic acid was extracted from gastric biopsies using a commercial kit (QIAGEN DNeasy tissue kit). H. pylori babA2 and iceA genes were amplified using extracted deoxyribonucleic acid (DNA) and primers by polymerase chain reaction (PCR). majority, (71.1%), of the study participants, were H. pylori positive when tested with urease-campylobacter-like organism (CLO). In total, 46 H. pylori urease CLO-positive samples were randomly analyzed by PCR for iceA, of which, 12 (26%) and 7 (15%) were found to have iceA1 and iceA2 respectively. Of the CLO-positive samples, 9 were randomly analysed for babA2 by PCR. Three samples were babA2 positive and 6 were babA2 negative. in Ghana, although H. pylori is endemic, iceA prevalence is rather low and probably exerts a limited effect on bacterial virulence. Further evaluation would be required, not only to determine association with other virulence factors but more importantly, inter-relationships with wider host and environmental factors that impact on disease pathogenesis.

Clinical manifestations and comorbid conditions in patients with chronic gastritis according to Helicobacter pylori CagA and VacA status

Objective — to determine the frequency of clinical manifestations and comorbidities in patients with Helicobacter pylori‑associated chronic gastritis, depending on the presence of H. pylori cytotoxin‑associated gene A and vacuolating cytotoxin A status. Materials and methods. This cross‑sectional study included 84 patients aged over 18 years with H. pylori‑associated chronic gastritis (CG). Patients were divided into two groups: 50 patients with the cytotoxin‑associated gene A (CagA) and vacuolating cytotoxin A (VacA) H. pylori strains and 34 patients with CagA‑ and VacA‑ H. pylori strains. H. pylori virulent strains (CagA+, VacA+) were detected using the polymerase chain reaction method. Solid‑phase enzyme‑linked immunosorbent assay (ELISA) was employed to detect immunoglobulins (IgA, IgG) against the CagA and VacA antigens of H. pylori. Analysis of medical records was conducted to assess clinical manifestations and the presence of comorbidities. Comorbid conditions were diagnosed using electrocardiography, abdominal ultrasound, and when necessary, computed tomography and magnetic resonance imaging, as well as videocolonoscopy. Statistical analysis was performed using the Stata 11 and Statistica 6 statistical software packages. Results. Patients with CagA+ and VacA+ H. pylori strains were more likely to have epigastric pain (60% vs. 35.3%, p=0.026) and constipation (52% vs. 20.6%, p=0.004) than patients with CagA‑ and VacA‑ H. pylori strains. Among the associated comorbid conditions in patients with H. pylori‑associated CG, the following were identified: gastroesophageal reflux disease — 33.3%, irritable bowel syndrome — 35.7%, non‑alcoholic fatty liver disease — 23.8%, autoimmune thyroiditis — 9.5%, arterial hypertension — 10.7%, and ischemic heart disease — 10.7%. The irritable bowel syndrome was significantly more prevalent in patients with CagA+ and VacA+ H. pylori strains, compared to those without CagA and VacA strains (46% vs. 20.6%, p=0.017). Other comorbid conditions occurred at similar frequencies among patients in both groups (p <0.05). Conclusions. Our study established that H. pylori virulent strains (CagA+, VacA+) could influence the clinical manifestations and associated conditions in patients with CG. Epigastric pain and constipation were more frequently observed in patients with H. pylori virulent strains (CagA+, VacA+), while the occurrence of irritable bowel syndrome was more pronounced among the associated conditions. The presence of H. pylori infection with CagA+ and VacA+ strains may be a risk factor for the development of irritable bowel syndrome. Eradication therapy could be considered as a preventive method for this comorbidity, but further research is needed to confirm this hypothesis.

Relationship between antibiotic resistance and the cagA and vacA genotypes among Helicobacter pylori strain isolates from patients in Xi'an.

The issue of drug resistance of Helicobacter pylori is becoming increasingly serious. To analyze the correlation between the cagA and vacA genotypes of H. pylori strains and their resistance to metronidazole, levofloxacin, and clarithromycin in patients in Xi'an, we studied 117 H. pylori strains isolated from patients in Xi'an. Antibiotic susceptibility testing of H. pylori was performed. The cagA and vacA genotypes were investigated using PCR. Among 117 strains of H. pylori, the rate of detection of cagA was 91.45% (107/117), among which the detection rate of East Asian-type cagA was 85.05% (91/107) and that of Western-type cagA was 14.95% (16/107). There were only two genotypes of vacA: s1m1 and s1m2. The detection rate of vacAs1m1 was 47.01% (55/117) and that of vacAs1m2 was 52.99% (62/117). The dominant strains in Xi'an were cagA + vacAs1m2 strains. The metronidazole resistance rate of vacAs1m2 H. pylori strains was significantly higher than that of vacAs1m1 H. pylori strains (91.94% vs. 69.09%, P = 0.002). The levofloxacin resistance rate of Western-type cagA strains was significantly higher than that of East Asian-type cagA strains (56.25% vs. 20.88%, P = 0.004). The metronidazole resistance rate of cagA + vacAs1m2 H. pylori strains was significantly higher than that of cagA + vacAs1m1 H. pylori strains (91.23% vs. 66.00%, P = 0.001). Our results showed that Western-type cagA strains were more likely to develop levofloxacin resistance than East Asian-type cagA strains. VacAs1m2 strains were more prone to metronidazole resistance than vacAs1m1 strains.

Prevalence and virulence factors of Helicobacter pylori isolated from oral cavity of non-disease, gastritis, and gastric cancer patients

Background/purposeThe oral cavity is considered a reservoir of Helicobacter pylori associated with gastric infection. It aimed to examine the prevalence of H. pylori strains from the oral cavity and gastric tissue of patients with different stage of gastric-diseases. Strains were further characterized for virulence genes, adhesion ability, and inflammation responses. Materials and methods11 non-disease, 15 gastritis, and 15 gastric cancer participated in the study. After clinical examination, gastric biopsies, saliva and plaque samples were collected and H. pylori levels were examined by real-time PCR and cultivation. The cagA and vacA genes were investigated from the culture strains. Adhesion ability and pro-inflammatory responses were analyzed in comparison between the presence of virulent genes and disease status. ResultsRelatively poor periodontal condition was found among gastric cancer patients. Prevalence of H. pylori-positive was 84.8% and 19.5% by real-time PCR and cultivation, respectively. The cagA and vacA gene-positive strains were 52.6% and 5.3%, respectively, which were found more in gastric cancer patients. The cagA gene-positive strains were found to be higher in gastric cancer patients, and strains had significantly higher adhesion ability and pro-inflammation expressions than the cagA gene-negative strains. ConclusionColonization by H. pylori in oral cavity was confirmed, and the cagA gene-positive strains play a crucial role in both adhesion and inflammatory responses. The presence of H. pylori and its virulence gene in oral cavity should be received attention. An eradication of such strains from oral cavity may help to prevent the transmission and recolonization to gastric organs.

Association between genetic polymorphisms of NOD1, Interleukin-1B, and cagA strain with low-grade duodenal eosinophilia in Helicobacter pylori-related dyspepsia.

Functional dyspepsia (FD) is a multifactorial disorder. Helicobacter pylori (H. pylori)-related dyspepsia (HpD) may be considered a separate entity. Duodenal eosinophilia is a potential pathogenic mechanism in FD. However, the impact of duodenal eosinophilia and host genetic polymorphism of innate and pro-inflammatory cascade, nucleotide-binding oligomerization domain 1 (NOD-1), and interleukin-1 beta (IL-1β) in HpD was not explored. To evaluate the association of NOD1-796G>A and IL-1B-511C>T gene variants and low-grade duodenal eosinophilia in HpD. A multicenter cross-sectional study was conducted. A total of 253 patients who met Rome-IV criteria were selected before upper endoscopy and 98 patients were included after unremarkable upper endoscopy and positive H. pylori in gastric biopsies were assessed. Clinical parameters, H. pylori cagA and duodenal histology, were evaluated. Sixty-four (65%) patients had epigastric pain syndrome (EPS), 24 (25%) postprandial distress syndrome (PDS), and 10 (10%) EPS/PDS overlap. FD subtypes were not associated with NOD1-796G>A and IL-1B-511C>T gene variants. Low-grade duodenal eosinophilia was significantly increased in NOD1-796 GG versus single A-allele, but not in IL-1B-511 single T-allele or CC-allele. This association is dependent of cagA infection, since harboring cagA strain was significantly associated with low-grade duodenal eosinophilia with isolated variants NOD1-796 GG and IL-1B-511 single T-allele, but not without cagA. When we performed combined polymorphism analysis with NOD1-796 GG/IL-1B-511 single T-allele, a synergistic effect on low-grade duodenal eosinophilia was found between these two loci irrespective of cagA strain status in HpD. Our findings suggest that low-grade duodenal eosinophilia is significantly associated with NOD1-796 GG allele specially in cagA strain and with allelic combination NOD1-796 GG/IL-1B-511 single T-allele independent of cagA strain infection in HpD patients.

Assessment of the mixed origin of the gastric epithelial extracellular vesicles in acellular transfer of Helicobacter pylori toxins and a systematic review

BackgroundH. pylori are generally considered as extracellular organisms, with exclusive colonization of the gastric milieu. Yet, several extra gastric manifestations are associated with this infection. The aim of the present study was to investigate the feasibility of toxin transfer by extracellular vesicles, from bacterial and epithelial origins. MethodsTox-positive H. pylori and its two cagA and vacA mutant strains were used to produce bacterial vesicles (BVs) and to infect AGS cells. The produced BVs and the infected cell vesicles (ICVs) were collected by ultracentrifugation and evaluated by western blotting, DLS and electron microscopy. These two sets of vesicles were applied to a second set of recipient AGS cells, in which the acellular transfer of toxins, IL-8 production and downstream morphologic changes were assessed, by western blotting, ELISA and light microscopy, respectively. ResultsThe BVs were positive for H. pylori membrane markers (BabA and UreB), VacA and CagA toxins, except for from the corresponding mutant strains. The ICVs were larger in size and positive for bacterial markers, as well as epithelial markers of CD9, LGR5, but negative for nuclear (Ki76) or cytoplasmic (β-actin) markers. Bacteria-independent transfer of CagA and VacA into the recipient cells occurred upon treatment of cells with BVs and ICVs, followed by cellular vacuolation and elongation. IL-8 production was induced in recipient AGS cells, treated with BVs (1279.4 ± 19.79 pg/106 cells), early (8 h, 1171.4 ± 11.31 pg/106 cells) and late (48 h, 965.4 ± 36.77 pg/106 cells) ICVs (P < 0.0001). ConclusionOur data indicates that ICVs, with mixed bacterial and epithelial constituents, similar to BVs, are capable of transferring bacterial toxins into the recipient cells, inducing IL-8 production and subsequent morphologic changes, in an acellular manner.

Low-grade duodenal eosinophilia is associated with cagA in Helicobacter pylori-related dyspepsia.

Functional dyspepsia (FD) is a multifactorial disorder. Helicobacter pylori (H. pylori)-related dyspepsia (HpD) may be considered a separate entity. Duodenal eosinophilia is a potential pathogenic mechanism in FD. However, the impact of duodenal eosinophilia and H. pylori virulence genes in HpD was not explored. We aim to evaluate the association of H. pylori virulence genes and low-grade duodenal eosinophilia in HpD. A multi-center cross-sectional study was conducted. A total of 301 patients who meet Rome-III criteria were selected before upper endoscopy, and 95 patients were included after normal endoscopy and positive H. pylori in gastric biopsies were assessed. Clinical parameters, H. pylori virulence genes (cagA, oipA, and vacA) and duodenal histology were evaluated. Sixty-nine (72%) patients had epigastric pain syndrome (EPS), 17 (18%) post-prandial distress syndrome (PDS) and 9 (10%) EPS/PDS overlap. FD syndromes were not associated with cagA or oipA strains. A significantly trend of vacA s1/m1 (78%) and s1/m2 (80%) positive strains in EPS was observed. Histological duodenal grading of chronic inflammation, low-grade duodenal eosinophilia and intra-epithelial lymphocytes showed no difference in oipA and vacA strains. Low-grade duodenal eosinophilia was significant in cagA positive strain, and the OR for low-grade duodenal eosinophilia with H. pylori cagA positive strain was 4.2 (95% CI, 1.78-9.93). Adjusting for age, gender, smoking, diabetes, alcohol, PPI, and NSAID, the OR was 5.44 (1.989-14.902). Our findings suggest that low-grade duodenal eosinophilia is significantly associated with cagA strain in HpD.

The effect of endogenous antimicrobial peptides (HNPs1-3 and LL-37) on the course of duodenal ulcer in children

Introduction. Duodenal ulcer in children is characterized by a significant prevalence, frequent development of serious complications and the need for large financial allocations for the implementation of treatment programs. Antimicrobial peptides have an immunomodulatory function and can be used as markers of the severity of the inflammatory process.Aim. To investigate the concentration of HNPs 1-3 and LL-37 in children with duodenal ulcer.Methods. A study of 47 children with duodenal ulcer, aged 7–18 years, was conducted with the determination of the CagA HR antigen in feces by enzyme-linked immunosorbent assay, the levels of HNPs 1-3 and LL-37 in blood plasma by enzyme-linked immunosorbent assay on the "PrisMatic" IN013 model 4301 analyzer test systems "MyBioSource, Inc.", USA. All children underwent a complex clinical and instrumental laboratory examination (topographic intragastric pH-metry, endoscopic examination with targeted biopsy for morphological examination and determination of HP). Results. 76.6% of people with DU were infected with HP. 80% had a toxigenic CagA strain of HP. In the vast majority of children with DU, small ulcerative defects were diagnosed. II and III degrees of inflammatory activity occurred with almost the same frequency (44.6% and 34% of people), while I degree occurred only in 21.3% of cases. The average level of HNP1-3 in children with DU was 46.56 ± 8.52 ng/ml, LL-37 - 269.9 ± 26.53 ng/ml. Direct probable connections between the levels of HNP1-3 and LL-37 and the severity of the course and the activity of the inflammatory process were established.Conclusion. Elevated levels of LL-37 and HNPs 1-3 were found in the blood plasma of children with duodenal ulcers associated with CagA strains of Helicobacter pylori. Significantly higher levels of LL-37 and HNPs 1-3 were registered with a severe course of the disease and an active inflammatory process, which indicates a direct influence of antimicrobial peptides on the course of the pathological process.

The effect of endogenous cortisol on the course of H.pylori-associated gastroduodenal diseases in adolescents

Background. The clinical picture and course of Н.pylori-dependent gastroduodenal diseases in adolescents have some characteristics, which complicate the diagnosis and treatment. The purpose was to investigate the level of cortisol in the blood of adolescents with Н.pylori-dependent gastroduodenal diseases. Materials and methods. A group of 96 patients (15–18 years old) was formed and divided into subgroups depending on the nosology (chronic gastroduodenitis, chronic erosive gastroduodenitis, duodenal ulcer) and gender. A comparison group included children of the same age. Fibroesophagogastroduodenoscopy was used to determine the endoscopic criteria for Helicobacter pylori (HP) and to perform a shield biopsy of the gastric mucosa (antrum and body of the stomach) and duodenum. HP infection was confirmed by enzyme immunoassay with qualitative and quantitative determination of IgG antibodies to HP in blood serum (UBI MAYIWELL™, USA). Evaluating the level of cortisol in the blood was carried out using a standard test system (Immunotech, Czech Republic). Results. The total frequency of HP detection was 54.2 %. It is worth noting that only 33.3 % of adolescents with H.pylori-associated gastroduodenal diseases have toxic CagA strains, while among patients with H.pylori-associated chronic erosive gastroduodenitis, such strains were detected in 70.8 % of cases. Children with duodenal ulcer are characterized by the highest number of HP strains in biopsies of the mucous membrane — 83.3 %. The level of cortisol in the blood of adolescents with pathology of the upper gastrointestinal tract was significantly higher than that in the comparison group (906.33 ± 43.56 nmol/ml and 666.21 ± 33.42 nmol/ml, respectively; p &lt; 0.05). The highest cortisol content in the blood was registered in patients with duodenal ulcer, with a predominance of higher indicators among adolescent boys. Significantly higher blood levels of cortisol were found in the stage of exacerbation and with a high degree of activity of the inflammatory process. Conclusions. In adolescence, inflammatory and destructive changes in the duodenal mucosa are potentiated by a high level of cortisol in the blood, it is higher in adolescent boys, with a high degree of inflammatory activity and in association with Helicobacter pylori infection.

S1234 Helicobacter pylori Infection and Cag-A Strain Are Associated With NAFLD Severity

S1234 Helicobacter pylori Infection and Cag-A Strain Are Associated With NAFLD Severity

The role of highly toxigenic CagA and VacA strains of Helicobacter pylori in gastric carcinogenesis. Review

Gastric cancer takes the 4th place as the main cause of death among oncological diseases in the world. The risk factors of gastric cancer include genetic predisposition, alcohol abuse, smoking, low socio‑economic level, nutritional characteristics, Epstein–Barr virus and Helicobacter pylori infection. Helicobacter pylori bacterium is the only statistically proven risk factor for stomach cancer. Gastric cancer develops in less than 3 % of ­H. pylori ‑infected patients, suggesting a unique interaction between the host immune response and H. pylori virulence factors. Expression of oncogenic cytotoxin‑associated protein gene A (CagA), vacuolating cytotoxin A (VacA), and outer membrane proteins is important for H. pylori in host pathogenesis. The paper gives consideration for the relationship between the virulence factors of H. pylori and the host, which is necessary for a better understanding of the pathogenesis and prevention of carcinogenesis. The strategy for the prevention of gastric cancer includes eradication therapy, but it is complicated by the growth of resistance to antimicrobial drugs. Only insignificant number of papers investigate effects of pathogenicity factors of H. pylori (CagA+ and VacA+) on the development of atrophy, intestinal metaplasia and dysplasia. In the literature, there is little data on the difference in antibiotic resistance between H. pylori highly toxigenic and non‑toxigenic strains. The aim of the article is to present current data on the impact of highly toxigenic CagA+VacA+ strains of H. pylori on the processes of gastric carcinogenesis and to determine their role in resistance to clarithromycin. Investigation of the relationship between highly toxigenic CagA and VacA strains with clinical and morphological manifestations of gastritis and antibiotic resistance will enable preventing the progression of precancerous changes and using effective treatment tactics.

Helicobacter Pylori-oncogenic protein cytotoxin-associated gene A and assessment of CD14 and CD163 in duodenal ulcer and gastric cancer patients

Nearly half of the world's population is infected with Helicobacter pylori (H.pylori). A duodenal ulcer or stomach cancer can be caused by the infection by this bacterium. The aim of this work is to assess the levels of CD14 and CD163 in H.Pylori-positive patients infected with duodenal ulcer (DU) and gastric cancer (GC) and determine the prevalence of Helicobacter Pylori-oncogenic protein cytotoxin-associated gene A strains (H.pylori-CagA). This study included 89 individuals distributed as follows: 20 healthy individuals as controls and 69 patients infected with H. Pylori have been divided as follows: 27 patients infected with H.pylori only (H.Pylori+), 22 H.pylori+DU and 20 H.pylori+GC. H. Pylori-oncogenic protein cytotoxin-associated gene A strains (H-pylori-CagA) were diagnosed based on a qualitative reverse-phase Enzyme Immunoassay Technique. CD163 and CD14 were measured in all individuals' serum using the Enzyme-Linked Immunoassay (ELISA) test. Out of 69 patients infected with H.pylori, there was one CagA strain in H.pylori+; two and five strains were recorded in H.pylori+DU and H.pylori+GC, respectively. CD14 and CD163 serum concentrations were significantly higher (P≤0.05) in H. pylori+, H. pylori+DU and H. pylori+GC than in controls. Conclusions: Patients with CagA strains infection are at risk of developing a duodenal ulcer and stomach cancer.

IMPROVEMENT OF ERADICATION THERAPY IN CHILDREN WITH DUODENAL ULCER ASSOCIATED WITH HELICOBACTER PYLORI

The aim: To evaluate the efficacy of the drug VitD children with H.pylori-associated duodenal ulcer. Materials and methods: Two treatment groups of children with DU were formed: I - 60 children with H. pylori-associated DU, who received the optimal scheme of anti- Helicobacter therapy (AHBT) for Chernivtsi region; II - 62 children with H. pylori-associated DU who received a modified treatment regimen: AGBT + VitD at a dose of 2000 IU / day for 1 month. The effectiveness of the treatment was evaluated taking into account the Relative Risk Reduction (RRR) of the adverse event and Number Needed to Treat (NNT). Results: All children with DU and a positive H. pylori infection test showed changes in serum VitD levels: 81.9% deficiency and 18.1% insufficiency. Successful eradication was achieved in 77.1% of children, in particular in the first group 73.3%, in the second - 82.2%. Predictors of successful eradication are the duration of infection, H. pylori CagA (+), VitD level. When using the VitD treatment regimen in children with DU associated with CagA (+) strain H.pylori, RRR was observed 2.29 times (χ2 = 6.34, pφ&lt;0.05) with NNT 1.59. Conclusions: Due to the reduced level of serum VitD in children with H. pylori-associated DU, it is advisable to include in the treatment regimen the adjuvant component of AHBT in the form of VitD. Predictors of effective eradication of H. pylori are CagA (+) strain of H. pylori, duration of infection and VitD level.

Clinical variants of chronic gastritis in childhood

Objective. To establish the features of various clinical variants of chronic gastritis in childhood.&#x0D; Material and methods. 415 children aged 617 years with chronic Hp-associated gastritis were examined. The clinical and anamnestic data, the results of laboratory, endoscopic and morphological studies of gastrobioptates were analyzed. Genetic typing of Hp was carried out with the determination of 16 pathogenicity factors. The persistence of human herpes viruses of types 6 and 8 and Epstein Barr viruses in the gastric mucosa was determined.&#x0D; Results. The clinical heterogeneity of chronic gastritis in children with the allocation of four topical variants was established: isolated duodenitis, duodenogastritis, antrum gastritis, pangastritis. It was found that with the first two, a high frequency of giardiasis is registered, with antrumgastritis and especially pangastritis, a significant contamination of the gastric mucosa with Hp is detected, mainly of CagA and VacA-positive strains. It is proved that the persistence of the type 6 human herpes virus does not affect the severity of inflammation, while the presence of the Epstein-Barr virus increases it. Colonization of the gastric mucosa by highly pathogenic Hp strains significantly increases the severity and activity of inflammation. It is shown that atrophy of the gastric mucosa in children is uncertain, and true atrophic gastritis occurs only in 0.61 % of cases.&#x0D; Conclusions. Chronic gastritis in children is a heterogeneous pathology, and its individual variants differ significantly in etiological factors including infectious, pathogenetic mechanisms and features of the morphology of gastric mucosa. This should be taken into account when carrying out medical support for patients.

Study on the Interaction of Algal Peptides on Virulence Factors of Helicobacter pylori: In Silico Approach.

In the Asian region, Helicobacter pylori infects about 80% populations, which is most leading cause of peptic ulcers, and it is an asymptomatic infection. Studies reported that the particular bacteria carry specific virulence factors that leads to severe complications. These virulence factors can be used as a drug targets to inhibit their growth and pathogenicity. Chronic infection with H. pylori virulence factors are CagA, VacA and HtrA positive strains the risk factor of gastric cancer. In this study, we aimed to study the antagonistic interaction pattern between the potential eight algal peptides against the virulence factors of H. pylori through in silico analysis intended to treat peptic ulcer and prevent the further complications such as cancer. The proteins of virulent factors are docked using C-Docker algorithm and calculated the bind energy of the complexes. The results showed that the peptide derived from a green alga, Tetradesmus sp. are active against the three virulent factors such as cag-A, vac-A, and Htr-A with multiple hydrogen, vdW, electrostatic interactions, and mild π-hydrophobic bindings with the libdock energy score for CagA, VacA and HtrA are 175.625, 158.603 and 89.397 kcal/mol. These primes and the peptide lead to develop a better and potential inhibitors against H. pylori infection.

Cytotoxin-associated gene A (CagA) promotes aortic endothelial inflammation and accelerates atherosclerosis through the NLRP3/caspase-1/IL-1β axis.

Atherosclerosis is a chronic inflammatory disease. Pathophysiological similarities between chronic infections and atherosclerosis triggered interests between these conditions. The seroepidemiological study showed that Helicobacter pylori strains that express cytotoxin-associated gene A (CagA), an oncoprotein and a major virulence factor, was positively correlated with atherosclerosis and related clinical events. Nevertheless, the underlying mechanism is poorly understood. In this study, the seroprevalence of infection by H. pylori and by strains express CagA assessed by enzyme-linked immunosorbent assay (ELISA) showed that the prevalence of CagA strains rather than H. pylori in patients was positively correlated with atherogenesis. Correspondingly, we found that CagA augmented the growth of plaque of ApoE-/- mice in the early stage of atherosclerosis and promoted the expression of adhesion molecules and inflammatory cytokines in mouse aortic endothelial cells (MAECs). Mechanistically, both si-NLRP3 and si-IL-1β mitigated the promoting effect of CagA on the inflammatory activation of HAECs. In vivo, the inhibition of NLRP3 by MCC950 significantly attenuated the promoting effect of CagA on plaque growth of ApoE-/- mice. We also propose NLRP3 as a potential therapeutic target for CagA-positive H. pylori infection-related atherosclerosis and emphasize the importance of inflammation in atherosclerosis pathology.

Biliary Migration, Colonization, and Pathogenesis of O. viverrini Co-Infected with CagA+ Helicobacter pylori.

Co-infection with the cagA strain of Helicobacter pylori exacerbates the pathology of human liver fluke Opisthorchis viverrini (OV) infection leading to cholangiocarcinoma. However, underlying mechanisms remain unclear. We report a significant increase in cagA-positive and cagA-negative H. pylori in the stomach, blood, bile, and in the OV worms of co-infected Syrian golden hamsters at one hour, three hours, and one month, post-infection, compared to hamsters infected with either OV or H. pylori alone. Except in the worms, H. pylori numbers declined at three months post-infection, particularly in the bile fluid of co-infected animals. Both strains of H. pylori were immunohistochemically detected in the tegument of the worm, as well as in the bile duct epithelium when co-infected with O. viverrine, but not in H. pylori infection alone. Interestingly, only the cagA-positive strain was detected in the gut of the worm. Co-infection between cagA-positive H. pylori and O. viverrini resulted in a more severe biliary pathology and decreased E-cadherin expression in vivo and in vitro than those of the cagA-negative strain. These data suggest that O. viverrini acts as a carrier of cagA-positive H. pylori and co-migrates to the bile ducts, whereas O. viverrini facilitates H. pylori colonization and enhances the biliary pathogenesis and carcinogenesis.

Impact of iron status and inflammatory indices on atherosclerotic burden of patients with helicobacter pylori infection and coronary arterial disease

Objective: Both inflammation and iron deficiency are suggested to be associated with coronary arterial diseases (CAD) and H. Pylori infection. The explanatory interaction depending on serum iron status and inflammatory biomarkers for the extent of atherosclerosis in H. Pylori infection is obscure. Therefore, we aimed to analyze the impact of iron Status and inflammatory indices on atherosclerotic burden of seropositive CAD patients with CagA (cytotoxin-associated gene A) strains of H. Pylori.&#x0D; Materials and Methods: This was an observational study of patients' undergone elective and urgent coronary angiography due to CAD. Serologic H. pylori infection status and iron status was determined in all of 293 subjects. Further seropositive patients were divided into groups to evaluate the extent of coronary atherosclerosis according to Syntax scoring system. Propensity score matching and covariate- adjusted multivariate logistic regression were used to adjust for baseline differences between study groups.&#x0D; Results: The odds ratio of positive serology for the presence of iron deficiency and acute coronary syndromes were 2.5 (95% CI (1.1-5.4); p = 0.02) and 3.0 (95% CI (1.3-7.0); p = 0.007) respectively. After controlling for diabetes mellitus, smoking, MPV, RDW and haemoglobin levels; Tsat ≤ 24.5 remained negatively associated with advanced atherosclerosis (OR:9.9, 95% CI (4.1-24.3); p &lt; 0.0001). In our matched sample, multivariable linear regression analysis showed that association of syntax score with Tsat was independent of hs-CRP (p=0.001).&#x0D; Conclusions: Irrespective of inflammatory status, transferrin saturation can be the decisive mirror indicator of advanced atherosclerosis in seropositive CAD patients with CagA strains of H. Pylori.

MODERN ASPECTS TO THE PROBLEM OF THE PREVALENCE OF HELICOBACTER PYLORI ASSOCIATED STOMACH DISEASES IN UZBEKISTAN

Introduction. We studied the regional epidemiological and genetic characteristics of the prevalence of Helicobacter pylori among the population of Uzbekistan. The work is based on the totality of the results of clinical, biochemical, immunological, genetic and instrumental research methods. Materials and Methods. It was established that Uzbekistan belongs to the regions with a high degree of H. pylori infection of the population (80%). 84% of the population of Uzbekistan have a mixed IceA1- / IceA2-genotype CagA. In peptic ulcer disease, the pathogenic strain CagA + VacA s1, VacA m2 and IceA 1,2 prevails, in chronic gastritis (type B) associated with H. pylori, the strain Cag + VacA s1, VacA m2 and IceA 1. Results and Discussion. The level of resistance of H. pylori strains to clarithromycin reaches 13.3%. Prolongation of eradication therapy up to 10 days and the addition of BTD to it makes it possible to increase the efficiency of H. pylori eradication up to 95%. Conclusion. Due to the presence of HP resistance to clarithromycin in 13.3% of cases and taking into account the low effectiveness of triadotherapy (72.5%), it is advisable to use quadritherapy with the inclusion of BTD in the standard of treatment, which contributes to an increase in the eradication efficiency up to 95%.