Search

Background Helicobacter pylori (H. pylori) is the causative agent of stomach diseases such as duodenal ulcer and gastric cancer, in this regard incomplete eradication of this bacterium has become to a serious concern. Probiotics are a group of the beneficial bacteria which increase the cure rate of H. pylori infections through various mechanisms such as competitive inhibition, co-aggregation ability, enhancing mucus production, production of bacteriocins, and modulating immune response. Result In this study, according to the received articles, the anti-H. pylori activities of probiotics were reviewed. Based on studies, administration of standard antibiotic therapy combined with probiotics plays an important role in the effective treatment of H. pylori infection. According to the literature, Lactobacillus casei, Lactobacillus reuteri, Lactobacillus rhamnosus GG, and Saccharomyces boulardii can effectively eradicate H. pylori infection. Our results showed that in addition to decrease gastrointestinal symptoms, probiotics can reduce the side effects of antibiotics (especially diarrhea) by altering the intestinal microbiome. Conclusion Nevertheless, antagonist activities of probiotics are H. pylori strain-specific. In general, these bacteria can be used for therapeutic purposes such as adjuvant therapy, drug-delivery system, as well as enhancing immune system against H. pylori infection.

Background: Helicobacter pylori (H. pylori) is one of the most common chronic bacterial infections in the world, and it is currently estimated that approximately half of the world's population is infected with the bacterium. The correct diagnosis and effective treatment of H. pylori gastric infection are essential in controlling this condition. The available diagnostic methods have advantages and limitations related to factors such as age of patients, technical difficulty level, costs and extensive accessibility in hospitals. The eradication therapy of H. pylori infection is still a challenge for gastroenterologists. One of the main causes of failure in H. pylori eradication is antibiotic resistance. Biopsy cultures are the most widely used methods among the antimicrobial susceptibility tests. Aim of Study: The aim of this work was to determine the proper regiment of H. Pylori treatment according to gastro-duodenal tissue culture and antibiotic sensitivity. Patients and Methods: This study included 50 patients with Helicobacter Pylori Ag positive stools and positive occult blood in stool. Their age ranged from 1.5 to 17 years old, 60% of them were female. 37 patients showed positive gastric and duodenal cultures and received treatment according to results of cultures. Results: Antibiotic sensitivity of gastric culture shows that Levofloxacin had the highest antibiotic sensitivity (93.5%), followed by clarithromycin and amoxicillin in (77%) and (67.7%) respectively. But, 100% of cases were resistant to the Metronidazole. In duodenal culture, Levofloxacin had the highest antibiotic sensitivity (96.4%), followed by, clarithro-mycin and amoxicillin in (71.4%) for each. But, 100% of cases were resistant to the Metronidazole. All patientsreceived PPI and Levofloxacin, while about 59% and 30% of patients received Amoxacillin and Clarithromycin respectively. Conclusion: Treatment of Helicobacter Pylori should be tailored according to tissue culture and sensitivity.

Objective Helicobacter pylori is one of the most common causes of gastric infections in humans. It is estimated that approximately 50% of people around the world are infected with this bacterium. This study aimed to determine the antibiotic resistance pattern, as well as the frequency of cagA and vacA genes in H. pylori isolates obtained from patients in the clinical centers in Tabriz city, Iran. Results The culture method detected 100 (45.25%) H. pylori isolates from 221 biopsy samples during 3 years. The results showed that 63% and 81% of the isolates were positive for cagA and vacA genes, respectively. The highest resistance of isolates was seen against metronidazole (79%) and amoxicillin (36%), respectively. Also, the isolates showed the least resistance to tetracycline (8%).

Garlic originated in West China and has been used for its health qualities since 2600 bc. Garlic was brought to Great Britain in 1548 from the Mediterranean Sea. Early uses of garlic were to treat gastric infections, fevers, and diarrhea. Fresh garlic has the most health benefits through the compound allicin. Health benefits of garlic include the prevention and treatment of cardiovascular disease, antioxidant effects, antimicrobial effects, and reduction of cancer risks.

Salama et al., in the current issue of Afro-Egypt J Infect Endem Dis published an interesting article focusing the prevalence of H pylori among patients with persistent itching. The authors reported a prevalence of H pylori among 130 out of 280 patients (46.4%) of persistent itching after exclusion of the common causes of itching. The authors reported 60% complete response defined as disappearance of itching after 2-weeks of H pylori treatment. Furthermore, 20% of patients reported partial improvement while 20% did not improve in comparison to 0% among the H pylori negative group treated with anti-histaminics. The authors reported also Ig E levels to be significantly higher among H pylori negative cases ruling out the allergic mechanism as a cause of skin affection in H pylori infected subjects.

Accumulating evidence indicates that persistent Helicobacter pylori gastric infection influences immune responses to oral enteric vaccines. We studied the association between pre-existing H. pylori serum IgG and serum pepsinogens levels (PGs) as markers of gastric inflammation and the immune response to single-dose live oral cholera vaccine CVD 103-HgR in Malian adults. Baseline sera obtained during a phase 2 safety/immunogenicity clinical trial of cholera vaccine CVD 103-HgR among 93 healthy Malian adults were tested for H. pylori IgG antibodies and PGI and PGII levels using enzyme linked immunosorbent assays. Overall 74/93 (80%) vaccine recipients were H. pylori IgG seropositive at baseline. Vibriocidal antibody seroconversion (≥ fourfold increase 14 days following administration of CVD 103-HgR compared to baseline) among vaccine recipients was 56%. However, vibriocidal antibody seroconversion was markedly higher among H. pylori seropositives than seronegatives 64% vs. 26% (p = 0.004); adjusted relative risk: 2.20 (95% confidence intervals 1.00–4.80; p = 0.049). Among H. pylori seropositive vaccine recipients, there were no significant associations between PGI, PGII and PGI:PGII levels and vibriocidal seroconversion. The enhanced seroconversion to oral cholera vaccine CVD 103-HgR among H. pylori seropositive African adults provides further evidence of the immunomodulating impact of H. pylori on oral vaccine immunogenicity.

Paediatric Menetrier disease (PMD) is a protein-losing gastropathy, presenting with generalized oedema and abdominal symptoms. PMD commonly has an acute course and may be associated with Cytomegalovirus (CMV) infection. The aim of this retrospective study is to assess the epidemiological and clinical data, diagnostic procedures, treatment and outcome of CMV-associated PMD. The medical charts of the patients with PMD and CMV infection diagnosed at our hospital have been reviewed. Then, a systematic literature's review of all the cases of PMD and a selection of those associated with CMV infection have been performed. Three previously healthy boys were admitted for vomiting and oedema. Endoscopy showed hypertrophic gastric folds and CMV infection was diagnosed. Albumin was administered in all cases, with clinical resolution within few weeks. In literature, PMD has been described in 150 children and the association between CMV and PMD was found in 89 cases. Clinical and laboratory data, radiological and histological exams, therapy and outcome were reviewed.Conclusions: Basing on the present experience and on the current knowledge, PMD has a benign course without long-term sequelae. Although PMD is rare in children, we recommend paediatricians to consider CMV-related PMD when facing children with vomiting and diffuse oedema. What is Known: • Paediatricians should consider Menetrier disease (MD) when facing oedematous child complaining of abdominal symptoms with hypoalbuminemia, without proteinuria and liver dysfunction. • Typical ultrasound features (hypertrophic gastric folds) suggest such condition which requires endoscopy and biopsy for definitive diagnosis. What is New: • A familial susceptibility to CMV gastric infection has been recently suggested; thus when suspecting MD, the family history of gastric diseases should be investigated. • Menetrier disease has been found associated with other unusual conditions either benign (such as gastric bezoar) or malign as neoplasms (acute lymphatic leukaemia and adenocarcinoma) even in children.

Periodontitis is a chronic degenerative disease which is inflammatory and whose bacteriological aetiology interests the hard and soft tissues supporting the dental elements. A typical characteristic of periodontitis is its correlation with other branches of medicine since periodontal disease is often associated with several other illnesses or systemic conditions which exacerbate or predispose the course of the disease. Amongst the most frequent gastroduodenal diseases are those associated with Helicobacter pylori (Hp) infections such as acute gastritis, chronic atrophic gastritis, gastric atrophy, gastritis ulcers, dysplasia, duodenal ulcer, gastric cancer, gastric MALT-lymphoma. Transmission of the microorganism occurs through iatrogenic pathways (faecal-oral, oral-oral) and through food and water ingestion. From this the possible role of the oral cavity becomes evident as a means of transmitting the microorganism and as an extra-gastric reservoir of Hp which develops inside the oral plaque, the main aetiological agent of periodontal disease. Considering that in a patient affected with periodontal disease the oral cavity presents elevated indices of bacterial plaque in association with infrabony pockets one is brought to ask if it might represent a favourable habitat for Hp colonisation. Furthermore, another query that one might pose is whether the presence of Hp in the oral cavity might be the cause of relapse in gastric infections caused by Hp. Consequently, might non-surgical periodontal treatment, in association with an eradicating gastric therapy, foster decontamination of the microorganism in the oral cavity leading to a better prevention of relapse and re-infection of the gastric cavity? Could non-surgical periodontal treatment thus mean prevention of gastric diseases brought on by Helicobacter pylori? The objective of this study is therefore to evaluate the incidence of periodontal disease and oral Hp infection in patients affected by gastric Hpinfection and to determine the possible benefits of the association of non-surgical periodontal therapy with eradicating gastric therapy compared with treatment that involves just the eradicating gastric therapy in patients who are affected by periodontal disease and Hp infection.

Review question / Objective: Is gastric helicobacter pylori infection related to periodontal diseases? Condition being studied: Therefore, the aim of this systematic review and meta-analysis was to identify and analyze clinical studies to determine the direct correlation between Helicobacter Pylori gastric infection andPeriodontal Disease. Study designs to be included: Clinical studies that provided data on Helicobacter Pylori infection in both the stomach and oral cavity, confirmed by polymerase chain reaction (PCR), rapid urease test (RUT) or enzyme-linked immunosorbent assay (ELISA). Clinical studies that associated PD with Helicobacter Pylori. The diagnosis of PD was confirmed ac-cording to the diagnostic criteria in periodontology.

Objectives This study was aimed to assess (1) the prevalence of salivary and gastric Helicobacter pylori (HP) infection in patients with and without periodontitis, (2) the prevalence of HP infection in patients with periodontitis according to its clinical classification, (3) the effect of periodontitis treatment in patients with or without gastric HP infection, and (4) if gastric HP eradication in combination with periodontitis treatment influences periodontitis clinical outcome. Materials and Methods Thirty-three adults with periodontitis treated by quadrant scaling and root planning (QSRP). The simplified plaque index (PI), bleeding on probing index (BOP), probing pocket depth (PPD), and clinical attachment level (CAL) were assessed pretreatment and 3 months of posttreatment. The patients were tested for oral and gastric HP. Gastric HP (+) patients received eradication therapy. A control group of 32 periodontically healthy volunteers was tested for oral and gastric HP. Saliva samples were evaluated by real-time polymerase chain reaction (rtPCR); gastric HP was detected by urea breath test (UBT). Statistical Analysis Normality of variables assessed by the Kolmogorov–Smirnov test, while the differences of pre- and post-treatment were analyzed by paired samples t-test. Differences between subgroups were compared by a Student’s t-test or a Mann–Whitney U-test. Comparisons of nominal variables were made by Pearson’s Chi-square test. Results No saliva samples were positive for HP. Gastric HP was detected in six patients with periodontitis and seven controls (p > 0.05). HP infection affected patients with higher disease stages and grades. All HP (+) patients underwent successful eradication treatment. All clinical periodontitis indices improved following QSRP. HP (+) patients who received QSRP as adjunctive to eradication treatment showed improvement in BOP (p < 0.001), PI (p < 0.013), and CAL (p < 0.004) compared with HP (−) patients who received QSRP alone. Conclusion Periodontitis was not associated with gastric HP infection. Saliva was not a gastric HP supply reservoir. Gastric HP infection was associated with advanced stages and grades of periodontitis. Although all periodontal clinical markers improved after QSRP, BOP, PI, and CAL, they were further improved when combined with eradication treatment. Periodontal evaluation and treatment combined with HP eradication are recommended in patients with HP gastric infection.

AimsEvaluate the rate and significance of Helicobacter pylori (H. pylori) involving duodenal foveolar metaplasia of chronic peptic duodenitis (CPD).MethodsWe identified 100 biopsy cases of CPD with synchronous stomach biopsies. All 200 were reviewed for histological changes (eg, chronic gastritis, acute inflammation) and underwent immunohistochemical staining for H. pylori. Results were correlated with patient age, sex, endoscopy indication and findings on stomach biopsy.ResultsCases included 49 men and 51 women, with a median age of 56 years. Reflux or dysphagia was the most common symptom. Chronic gastritis was present in 46 stomach biopsies, with 54 within normal limits. Twelve stomach biopsies showed H. pylori, all of which showed gastritis. Two duodenal biopsies (2%) demonstrated H. pylori organisms on immunohistochemistry, both from patients with H. pylori gastritis.ConclusionsRoutine examination of CPD samples for H. pylori appears unnecessary if a stomach biopsy is available for review.

Objective: To evaluate the correlation between the presence of H. pylori in paired samples of tap water and gastric cancer (GC) lesion in Lima city (Peru). Material and methods: Gastric tissue and tap-water samples were prospectively collected from 82 Gastric Cancer who lived in Lima. HspA and ureA genes were evaluated by qPCR in the samples. Results: The median age of patients with GC was 63 years, 52.4% were men and stage-II in 36.6%. A home-living time> 10 years was reported in 84.1% of patients. Boiling water treatment was indicated in 85.4% of cases. H. pylori was detected in 69.5% of gastric tissues and in 12.2% of analyzed tap-water. There was no differences in gastric infection rates among those with or without water contamination (70% vs. 69.4%, p=0.971). Conclusion & Impact: H. pylori was found in tap-water samples, however, detection rates were lower than in gastric cancer samples. Other sources of infection transmission should be investigated.

Helicobacter pylori (H. pylori) is a gram-negative bacterium that infects approximately 4.4 billion individuals worldwide. However, its prevalence varies among different geographic areas, and is influenced by several factors. The infection can be acquired by means of oral-oral or fecal-oral transmission, and the pathogen possesses various mechanisms that improve its capacity of mobility, adherence and manipulation of the gastric microenvironment, making possible the colonization of an organ with a highly acidic lumen. In addition, H. pylori presents a large variety of virulence factors that improve its pathogenicity, of which we highlight cytotoxin associated antigen A, vacuolating cytotoxin, duodenal ulcer promoting gene A protein, outer inflammatory protein and gamma-glutamyl transpeptidase. The host immune system, mainly by means of a Th1-polarized response, also plays a crucial role in the infection course. Although most H. pylori-positive individuals remain asymptomatic, the infection predisposes the development of various clinical conditions as peptic ulcers, gastric adenocarcinomas and mucosa-associated lymphoid tissue lymphomas. Invasive and non-invasive diagnostic methods, each of them with their related advantages and limitations, have been applied in H. pylori detection. Moreover, bacterial resistance to antimicrobial therapy is a major challenge in the treatment of this infection, and new therapy alternatives are being tested to improve H. pylori eradication. Last but not least, the development of effective vaccines against H. pylori infection have been the aim of several research studies.

Gastric infections are mostly triggered by Helicobacter pylori (H. pylori), a fungus that colonizes the stomach mucosa of more than 50% of the inhabitants of the world. Chronic H. Pylori diseasewas associated with stomach diseases such as peptic ulcer, chronic gastritis and stomach adenoc arcinoma. Current therapy for eradication relies on antibiotic-based therapies that are ineffective in about 20% of patients. Traditional method constraints optimize the creation of new techniques for fast, consistent and cost-effective H diagnosis. Infection with pylori. Wide-ranging study has been carried out over the previous few centuries to create a type of gastro-retentive dosage (GRDF). This sort of dosage form can advance the delivery and efficiency of stomach-active medicines because the GRDF enables the medication to remain in the stomach for a sufficient time period. Various methods were used to develop effective GRDFs such as high-density systems, low-density systems, swelling and expansion systems, hydrodynamically balanced systems, superporous hydrogels,. However, there are both merits and demerits in these kinds of schemes. Intra-individual and inter-individual dissimilarities are obstacles to the growth of effective GRDFs in gastric physiology. Examples of these individual differences include gastric pH and gastric motility that have a notable effect on the moment of stomach retention and delivery of drugs. Some of these obstacles can be overcome by developing a novel mucoadhesive microsphere. The mucoadhesive microsphere is characterized by close contact of the MDF with the mucosal layer, thereby increasing the localized absorption of the drug. H2Receptor antagonists (H2RAs) have become first-line therapy for acid related peptic disease and GRDF especially designed for H2RAs and drugs against H. pylori, including specific targeting systems and leading to a marked development in the quality of life for a large number of patients. In this relationship, new formulations with improved absorption, improved bioavailability and improved acid-suppressing regimens are welcome Keywords: H. pylori, gastro-retentive dosage, mucoadhesive microsphere

Background The global prevalence of H. pylori approaches 50%, with prevalence rates between 20 and 40% in developed countries and up to 90% in Africa and other developing nations of the world. Development of H. pylori-associated diseases is determined by a number of virulence factors. This study aimed at determining the prevalence of H. pylori infections and virulence genes (cagA, dupA, and vacA); the relationship between virulence factors and gastroduodenal diseases among patients. Methods Gastric biopsies were obtained from patients and cultured, DNA was extracted from cultured isolates and biopsies for PCR assay after which samples were investigated using standard laboratory procedures. Data of associated risk factors were obtained with the aid of questionnaires. Results Of the 444 participants, H. pylori was detected in 115 (25.9%) from culture analysis and 217 (48.9%) by direct PCR method. Ninety-eight (85.2%) of the culture-positive patients were also detected by PCR giving an overall prevalence of 52.7% (234/444). The highest number of H. pylori isolates 76.9% (180/234) was obtained from patients suffering from pangastritis. The CagA virulence gene was found in 62% (145/234), dupA in 53.4% (125/234) and vacA in 90.6% (212/234). VacA genotype s1 m1 was the most prevalent [56.4% (132)] followed by s2 m2 [11.5% (27)], s2 m1 [10.3% (24)] and [s1 m2 9.4% (22)]. There was a significant association observed in vacA s1 and peptic ulcer disease, as well as vacA s1/m2 and gastric erosion (P

Despite being one of the most studied cancer-related infections, the relationship between Helicobacter pylori infection and gastric adenocarcinoma (GC) remains, in some points, obscure. Based on a critical analysis of the available literature regarding stomach microbiota, we aimed to shed light to a possible new interpretation of the current understanding about the Helicobacter pylori-related GC carcinogenesis. We analyzed data from the literature on Helicobacter pylori and other potential carcinogenic pathogens, in both benignant conditions and gastric adenocarcinoma. Helicobacter pylori is the dominant microorganism in benignant conditions as non-complicated gastritis. In atrophic gastritis, metaplasia and, mainly, in gastric adenocarcinoma, a strong reduction in Helicobacter pylori abundance, and increased occurrence of other microorganisms is strongly demonstrated by metagenomic experiments. While causing peptic disease and keeping the stomach's high acidity, Helicobacter pylori infection avoids gastric infection by carcinogenic intestinal microbiota. Nevertheless, Helicobacter pylori persistence may also provoke an atrophic gastritis, a condition that causes its own decline, due to a microenvironment modification, including reduced acidity, resulting in Helicobacter pylori substitution by a cancer-prone microbiota. This new interpretation might result in a dramatic modification on clinical management of Helicobacter pylori-related gastric disease.

Background Peptic ulcer disease (PUD) is a common disease worldwide moreover known as stomach ulcer or peptic ulcer. Increased the number of T CD4+ helper cells in response to gastric infection by Helicobacter pylori (H. pylori) play an important role in the development of PUD. The aim of this study was to determine the frequency of T-bet+ cells in H. pylori-infection, its interaction with Th17/Treg cells and its association with the clinical consequences of the infection. Methods A total of 63 patients with PUD, 89 patients with gastritis and 48 H. pylori-negative subjects were enrolled in this study. The number of T-bet+ cells were determined by immunohistochemistry. Results The numbers of T-bet+ cells and INF-γ expression in infected patients were significantly higher than uninfected. Moreover, the number of T-bet+ cells and INF-γ expression in infected patients with PUD were significantly higher than infected patients with gastritis. Additionally, the number of T-bet+ cells and INF-γ expression were found to be inversely correlated with degree of H. pylori density and chronic inflammation score (CIS) in infected patients with gastritis disease, but this correlation was positive in the infected patients with PUD. The number of T-bet+ cells was found to be positively correlated with the number of Th17 cells and inversely correlated with the number of Treg cells in infected patients with gastritis and PUD. Conclusion Abnormal hyper-activation of T-bet+ cells during H. pylori-infection may lead to tissue damage caused by immunopathologic reactions.

Bacterial communities are known to impact human health and disease. Mixed species biofilms, mostly pathogenic in nature, have been observed in dental and gastric infections as well as in intestinal diseases, chronic gut wounds and colon cancer. Apart from the appendix, the presence of thick polymicrobial biofilms in the healthy gut mucosa is still debated. Polymicrobial biofilms containing potential pathogens appear to be an early-warning signal of developing disease and can be regarded as a tipping point between a healthy and a diseased state of the gut mucosa. Key biofilm-forming pathogens and associated molecules hold promise as biomarkers. Criteria to distinguish microcolonies from biofilms are crucial to provide clarity when reporting biofilm-related phenomena in health and disease in the gut. ISSN:0966-842X

Cathepsin C (CtsC) functions as a central coordinator for activation of many serine proteases in immune cells. However, CtsC expression in gastric epithelial cells and its role in Helicobacter pylori infection remain unclear. Real-time PCR, Western blot, and immunohistochemistry analyses identified that CtsC was decreased in gastric mucosa of H. pylori-infected patients and mice. Isolated gastric epithelial cells and cell lines were stimulated with H. pylori and/or TGF-β1 showed that down-regulation of CtsC in gastric epithelial cells largely depended on H. pylori cagA via Src/ERK and Janus kinase (JAK)/signal transducer and activator of transcription 3 (STAT3) pathways, and the effect could be synergistically augmented by TGF-β1 in an autocrine manner. In human gastric mucosa, CtsC expression was negatively correlated with bacteria colonization; accordingly, provision of exogenous active CtsC overwhelmed H. pylori persistence in gastric mucosa of mice. In the presence of active CtsC, isolated human neutrophils activated via NF-κB pathway with augmented bactericidal capacity in vitro. We also found that neutrophils activated and cleared bacteria in active CtsC-injected mice and that there was no bactericidal capacity in mice that were simultaneously neutrophil-depleted by Ly6G antibody. Our findings identified a mechanism that H. pylori abrogate CtsC to impair neutrophil activation and to ensure persistence in gastric mucosa. Efforts to enable and boost this neutrophil activation pathway by active CtsC may therefore become valuable strategies in treating H. pylori infection.-Liu, Y. G., Teng, Y. S., Cheng, P., Kong, H., Lv, Y. P., Mao, F. Y., Wu, X. L., Hao, C. J., Chen, W., Yang, S. M., Zhang, J. Y., Peng, L. S., Wang, T. T., Han, B., Ma, Q., Zou, Q. M., Zhuang, Y. Abrogation of cathepsin C by Helicobacter pylori impairs neutrophil activation to promote gastric infection.

PurposeGastric infection withStrongyloides stercoralis(SS) usually occurs in immunocompromised patients. The unexpected observation of this parasite in an otherwise healthy young lady who had undergone upper endoscopy and biopsy sampling of the gastro-duodenal mucosa, prompted us to review the literature to ascertain the conditions favouring gastric colonization bySS.MethodsPathology files of gastroduodenal biopsies received at St. Mary’s hospital, Northern Uganda, between 2007 and 2017 were reviewed. Pubmed search was performed under the headings “Strongyloides stercoralis”, “Gastric parasitosis”.ResultsHistology of the only gastroduodenal biopsy with SS infection showed parasite eggs, immature rhabditiform larvae, and numerous adult worms in gastric pits and rhabditiform larvae in interepithelial parasitic tunnels, causing reactive changes of the glandular epithelium. There was no significant acute inflammatory cell infiltrate surrounding the parasites. Literature review showed that gastricSSinfection appears to be very uncommon and was, as expected, largely prevalent in immunodeficient individuals (84.2% of published cases). The rare gastricSSinfection is a complication of systemic strongyloidiasis, either hyperinfective, or disseminated form. It is also commonly associated with duodenal infection at microscopical examination.ConclusionInvolvement of gastric mucosa in the absence of duodenal strongyloidiasis appears to be quite rare and false-negative histopathological exams are reported if only the stomach is biopsied.

Background Acute infective gastroenteritis (AIG) is a leading cause of mortality in children worldwide. In Peru, more than 40% of cases of AIG occurring in children under 5 years old. The disruption of the gut microbiota can increase risk for several health complications especially in patients with gastric infections caused by viruses or bacteria. Objective The main objective of this study was to describe the prevalence of 13 representative bacteria from the gut microbiota (GM) in stools samples from children under 5 years of age with acute infective gastroenteritis. Results The most commonly isolated bacteria from the GM were Firmicutes (63.2% 74/117) Bacteriodetes (62.4%; 73/117), Lactobacillus (59.8%; 70/117), Prevotella (57.2%; 67/117), Proteobacterium (53.8%; 63/117), regardless of the etiological agent responsible for the AIG. Interestingly, despite the high prevalence of Firmicutes, Bacteroidetes, Lactobacillus and Prevotella across all samples, a visible reduction of these agents was observed especially among patients with a single bacterial infection or even bacteria–bacteria coinfections when compared to viral etiologies. Patients with exclusive or mixed breastfeeding registered the highest amount of gut microbiota bacteria, in contrast to infants who received formula or were not breastfed.

BACKGROUND: Helicobacter pylori (H. pylori) is a Gram-negative bacteria and has been known for its role in causing gastric infection aused diseases such as gastric ulcer. H. pylori also implied to play a role in chronic tonsillitis, but this theory remains controversial. Many researches have different and contradictory results due to difficulty to accurately detect H. pylori in tonsillar tissue. There is still no appropriate method that able to detect H. pylori in tonsil tissue. AIM: The aim of the study was to detect H. pylori colonization in chronic tonsillitis and understand some of the methods of examination that can be done to detect H. pylori in tonsillar tissue. METHODS: This study is a descriptive study conducted on 25 respondents. Each sample was taken from patients with chronic tonsillitis who underwent tonsillectomy. Then, the rapid urease test (RUT) and the Giemsa modification staining were carried out to determine the presence of H. pylori. RESULTS: There were 19 people (76%) positive and 6 people (24%) negative for H. pylori using RUT. On examination with Giemsa modification staining obtained 19 people (76%) positive and 6 people (24%) negative for H. pylori. CONCLUSION: H. pylori can be found in most of chronic tonsillitis. Combination RUT and Giemsa modification staining examination can be a good option in detecting H. pylori in chronic tonsillitis.

Infection of the human stomach byHelicobacter pyloriremains a worldwide problem and greatly contributes to peptic ulcer disease and gastric cancer. Without active intervention approximately 50% of the world population will continue to be infected with this gastric pathogen. Current eradication, called triple therapy, entails a proton-pump inhibitor and two broadband antibiotics, however resistance to either clarithromycin or metronidazole is greater than 25% and rising. Therefore, there is an urgent need for a targeted, high-specificity eradication drug. Gastric infection byH. pyloridepends on the expression of a nickeldependent urease in the cytoplasm of the bacteria. Here, we report the 2.01 Å resolution structure of the 1.1 MDa urease in complex with a novel inhibitor by cryo-electron microscopy and compare it to a β-mercaptoethanol-inhibited structure at 2.45 Å resolution. The structural information is of sufficient detail to aid in the development of inhibitors with high specificity and affinity.

Coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is a global public health emergency. COVID-19 typically manifests as a respiratory illness but an increasing number of clinical reports describe gastrointestinal (GI) symptoms. This is particularly true in children in whom GI symptoms are frequent and viral shedding outlasts viral clearance from the respiratory system. By contrast, fetuses seem to be rarely affected by COVID-19, although the virus has been detected in placentas of affected women. These observations raise the question of whether the virus can infect and replicate within the stomach once ingested. Moreover, it is not yet clear whether active replication of SARS-CoV-2 is possible in the stomach of children or in fetuses at different developmental stages. Here we show the novel derivation of fetal gastric organoids from 8-21 post-conception week (PCW) fetuses, and from pediatric biopsies, to be used as an in vitro model for SARS-CoV-2 gastric infection. Gastric organoids recapitulate human stomach with linear increase of gastric mucin 5AC along developmental stages, and expression of gastric markers pepsinogen, somatostatin, gastrin and chromogranin A. In order to investigate SARS-CoV-2 infection with minimal perturbation and under steady-state conditions, we induced a reversed polarity in the gastric organoids (RP-GOs) in suspension. In this condition of exposed apical polarity, the virus can easily access viral receptor angiotensin-converting enzyme 2 (ACE2). The pediatric RP-GOs are fully susceptible to infection with SARS-CoV-2, where viral nucleoprotein is expressed in cells undergoing programmed cell death, while the efficiency of infection is significantly lower in fetal organoids. The RP-GOs derived from pediatric patients show sustained robust viral replication of SARS-CoV-2, compared with organoids derived from fetal stomachs. Transcriptomic analysis shows a moderate innate antiviral response and the lack of differentially expressed genes belonging to the interferon family. Collectively, we established the first expandable human gastric organoid culture across fetal developmental stages, and we support the hypothesis that fetal tissue seems to be less susceptible to SARS-CoV-2 infection, especially in early stages of development. However, the virus can efficiently infect gastric epithelium in pediatric patients, suggesting that the stomach might have an active role in fecal-oral transmission of SARS-CoV-2.

The Gram-negative gastric bacterium Helicobacter pylori is recognized as a class I carcinogen by the World Health Organization. Around 1% of infected individuals develop gastric cancer; this is a huge burden, given that over half the world’s population is chronically infected with this extraordinarily well adapted pathogen. Attempts to develop a vaccine began not long after the discovery of H. pylori in 1983, but although several strategies for both therapeutic and prophylactic vaccination have been partially encouraging in rodent models, protection in the native human host has been disappointingly inefficient. It has been shown that H. pylori has multiple strategies for suppressing T cell maturation. However, with the more recent discovery of new escape mechanisms that cause a blockage of epithelial effector functions, it is becoming clear why previous strategies for boosting T cell immunity have been ineffective. Accordingly, inflammatory cytokines released from recruited immune cells are unable to activate infected epithelial cells at the front line of defense, a mechanism that establishes a protected niche for the pathogen on the mucosal surface. In this chapter, we review the H. pylori vaccine field in light of these new findings, which may point the way toward novel unconventional strategies of immune protection against gastric infections as well as carcinogenesis.

Oral cavity has been taken as one of the major reservoirs for Helicobacter pylori, the bacteria responsible for gastric infection and cancers. Dentists are frequently exposed to saliva; thus, theoretically, they are at a higher risk for oral H. pylori infection. In the present study, to test this hypothesis and to find out the potential factors associated with the increased risk, a cross-sectional study was carried out on a large scale of dentists (N=90) and nondentist controls (N=110). By using nested polymerase chain reaction to amplify a specific DNA fragment of H. pylori, we found 7.27% of saliva samples from the nondentist group and 16.67% of saliva samples from the dentist group were oral H. pylori positive, and the difference between groups was statistically significant (χ2=4.292, p=0.038). Importantly, however, after stratifying enrolled subjects with factors which might interfere with the comparison of H. pylori detection rate between groups, we still observed a higher H. pylori frequency in the dentists than that in the controls in subgroups, including those with good individual hygiene, healthy lifestyle, and physical condition, as well as those living with families to be gastric disease free and not sharing meals with H. pylori-positive persons, respectively. Moreover, the frequency of clinical practice per week of the investigated dentists was closely associated with an oral H. pylori infection risk. Our data indicates that dentists are at a higher risk for H. pylori infection, and intensive attention needs to be paid on this issue.

Background The purpose of this study was to investigate the pathohistological status of mucous lining infected with Helicobacte pylori as the possible cause of chronic laryngitis and laryngeal carcinoma. Materials and methods The prospective examination included 51 patients suffering from planocellular laryngeal cancer and 26 examinees suffering from chronic laryngitis. The examinees and the control group were subjected to esophagogastroduodenoscopy which described the local status of the esophagus and stomach. Two biopsy samplings are taken from the stomach antrum and corpus. One part of the biopsies was colored using the histological technique used in the pathohistological detection of H. pylori, while the other part was incorporated in paraffin cubes where the H. Pylori gene expression was determined using the deparaffinization and PCR method DNA isolation. Results In the group of examinees suffering from laryngeal tumor, there were a higher number of patients suffering also from chronic gastritis (32/51) than in the other group, suffering from chronic laryngitis (9/26). In the chronic laryngitis group, there were more examinees with acute gastritis (12/26) than in the examined group (11/51). The difference is statistically significant (p = 0.0457). Conclusion Chronic gastritis and H. pylori infection are risk factors for laryngeal carcinoma formation ; therefore, acute gastritis with helicobacter pylori infection must be immediately treated to not let infection to become chronic.

Helicobacter pylori has been proposed as a possible etiologic factor of ocular adnexa lymphoma (OAL), although with conflicting results. To assess the involvement of H. pylori in OAL, as (1) H. pylori DNA positivity on OAL specimens, and (2) prevalence of H. pylori gastric infection in patients with OAL. A systematic review of studies assessing H. pylori in patients with OAL was conducted by searching electronic databases from their inception to May 2019. Pooled positivity for H. pylori in OAL specimens detected by polymerase chain reaction, and pooled prevalence of H. pylori gastric infection, were calculated with 95% confidence interval (CI). Eleven studies with 308 patients were included. Pooled positivity for H. pylori was 16.8% in all OALs and 22.7% in MALT OAL, with high heterogeneity among studies. Pooled prevalence of H. pylori gastric infection in patients with OAL was 34.7%, with low statistical heterogeneity. In conclusion, H. pylori seems to be involved in a subset of OAL, but the heterogeneity found needs to be investigated in further studies. The prevalence of H. pylori gastric infection in patients with OAL does not seem to differ from that of the general population.

Spirocerca lupi (family: Spirocercidae; order: Spirurida) are parasitic nematodes found in the esophagus of cats and dogs, as well as in other carnivore animals throughout the tropical, subtropical, and temperate countries of Asia and the Americas. These animals become infested by eating an intermediate host or a transport host. In adult felines, this parasite often resides in the mucosa of the esophagus, where it forms granulomatous nodules. In this work, a wild immature female Pallas’s cat (Otocolobus manul) that was younger than 1 year old was killed by a herding dog (heeler) in Mashhad, Iran. After necropsy, parasite samples were gathered from the stomach and after clarification by lactophenol, the nematodes were recognized as Spirocerca lupi. Microscopic diagnoses in the stomach include granulomatous nodules, mucosal gland destruction, necrosis, and inflammatory cell infiltration. This report characterizes the first documented case of spirocercosis in a Pallas’s cat in the world.

International audience; Persistent Helicobacter pylori (H. pylori) infection is related to 90% of gastric cancers. With bacterial resistance rising and treatment inefficiency affecting 15% of the patients, alternative treatments urge. Chitosan microspheres (ChMics) have been proposed as an H. pylori-binding system. This work evaluates ChMics biocompatibility, mucopenetration and capacity to treat H. pylori infection in mice after oral administration. ChMics of different size (XL, ∼120 µm and XS, ∼40 µm) and degree of acetylation (6% and 16%) were developed and revealed to be able to adhere both human and mouse-adapted H. pylori strains without cytotoxicity towards human gastric cells. Ex vivo studies showed that smaller (XS) microspheres penetrate further within the gastric foveolae, suggesting their ability to reach deeply adherent bacteria. In vivo assays showed 88% reduction of infection when H. pylori-infected mice (C57BL/6) were treated with more mucoadhesive XL6 and XS6 ChMics. Overall, ChMics clearly demonstrate ability to reduce H. pylori gastric infection in mice, with chitosan degree of acetylation being a dominant factor over microspheres' size on H. pylori removal efficiency. These results evidence the strong potential of this strategy as an antibiotic-free approach to fight H. pylori infection, where microspheres are orally administered, bind H. pylori in the stomach, and remove them through the gastrointestinal tract. STATEMENT OF SIGNIFICANCE: Approximately 90% of gastric cancers are caused by the carcinogenic agent Helicobacter pylori, which infects >50% of the world population. Bacterial resistance, reduced antibiotic bioavailability, and the intricate distribution of bacteria in mucus and within gastric foveolae hamper the success of most strategies to fight H. pylori. We demonstrate that an antibiotic-free therapy based on bare chitosan microspheres that bind and remove H. pylori from stomach can achieve 88% reduction of infection from H. pylori-infected mice. Changing size and mucoadhesive properties, microspheres can reach different areas of gastric mucosa: smaller and less mucoadhesive can penetrate deeper into the foveolae. This promising, simple and inexpensive strategy paves the way for a faster bench-to-bedside transition, therefore holding great potential for clinical application.

Helicobacter pylori (H. pylori) gastric infection is considered one of the most common human infections. It occurs in half of the world’s population is the most common cause of adenocarcinoma of the distal stomach [1]. [...]

Gastric cancers are a group of highly aggressive malignancies with a huge disease burden worldwide. Gastric infections, such as helicobacter pylori, can induce the occurrence of gastric cancers. However, the role of gastric infection in gastric cancer development is unclear. Programmed death-ligand 1 (PD-L1, B7-H1) is a member of the B7 family of cell surface ligands, which binds the PD-1 transmembrane receptor and inhibits T-cell activation within cancer tissues. It has been reported that the expression of PD-L1 is inversely related to the prognosis of patients with gastric cancers. Therefore, the regulation of PD-L1 expression in gastric cancers needs to be studied. In the current study, we explored the possible effects of lipopolysaccharide (LPS) on PD-L1 expression in gastric cancer cells. We observed that LPS stimulation could markedly increase PD-L1 expression in gastric cancer cells. Furthermore, we found that nuclear factor-κB (NF-κB) activation was involved in PD-L1 expression in gastric cancer cells exposed to LPS stimulation through p65-binding to the PD-L1 promoter. Taken together, these data indicate that gastric infection might promote the development of gastric cancers thought the LPS-NF-κB-PD-L1 axis.

Helicobacter pylori infection is one of the major risk factors for gastric cancer development. Available antibiotic-based treatments not only fail in around 20% of patients but also have a severe negative impact on the gut microbiota. Recently, we demonstrated that nanostructured lipid carriers (NLC), even without any drug loaded, are bactericidal against H. pylori at low concentrations. This work aims to clarify NLC mode of action and to evaluate if their bactericidal effect is specific to H. pylori without affecting bacteria from microbiota. NLC were produced by hot homogenization followed by ultrasonication method, using Precirol®ATO5 and Miglyol®812 as lipids and Tween®60 as a surfactant. NLC were able to eradicate H. pylori without affecting the other tested bacteria (Lactobacillus, E. coli, S. epidermidis and S. aureus). Bioimaging assays demonstrated that NLC rapidly bind to and cross the H. pylori bacterial membrane, destabilizing and disrupting it, which leads to leakage of the cytoplasmic contents and consequent bacterial death. In an era where efficient alternatives to antibiotics are urgent, NLC are an interesting route to be explored in the quest for new antibiotic-free therapies to fight H. pylori infection.