scholarly journals The Presence of Periodontal Pathogens in Gastric Cancer

2020 ◽  
Author(s):  
Marcel A. de Leeuw ◽  
Manuel X. Duval
Keyword(s):  
Gastric Cancer ◽  
Gastric Mucosa ◽  
Eradication Therapy ◽  
Downstream Processing ◽  
Data Sets ◽  
Periodontal Pathogens ◽  
Public Data ◽  
H Pylori ◽  
Pathogen Spectrum

BackgroundThe microbiome is thought to play a role in the development of gastric cancer (GC). Several studies have put forward putatively carcinogenic species in addition to Helicobacter pylori, but are not in perfect alignment, possibly due to variable parameters in the experiments, including downstream processing. Meta-analyses have not been published so far, so there is lack in clinical guidance beyond H. pylori eradication therapy.MethodsHere, we analysed gastric mucosa samples from nine public data sets, including GC samples. Using both unsupervised and supervised learning, we defined fine grain bacterial networks of gastric mucosa and identified species associated with tumor status of samples.ResultsWe found anatomic locations and cohort regions among the possible factors leading to the observation of study specific gastric microbiomes. Despite this variability, the periodontal species Fusobacterium nucleatum, Parvimonas micra and Peptostreptococcus stomatis were found in association with tumor status in several datasets. The three species were predicted to be in interaction by ecological network analysis and also formed the intersection of tumor associated species between four GC data sets and five colorectal cancer (CRC) data sets we reanalyzed. We formulated a probiotic composition putatively competing with the GC pathogen spectrum, from correlation analysis in a large superset of gut samples (n=17,800) from clinical- and crowd-sourced studies.ImplicationsThe overlapping bacterial pathogen spectrum between two gastrointestinal tumor types, GC and CRC, has implications for etiology, treatment and prevention. In vitro testing results reported in literature suggest H. pylori eradication treatment should be efficient against the GC pathogen spectrum, yet the existence of an upstream periodontal reservoir is of concern. To address this, we propose longer term use of the formulated probiotics composition.

scholarly journals Potential Association of EEF1A Dimethylation at Lysine 55 in the Basal Area of Helicobacter Pylori-Eradicated Gastric Mucosa with the Risk of Gastric Cancer: A Retrospective Observational Study

2021 ◽  
Author(s):  
Yuka Hirashita ◽  
Masahide Fukuda ◽  
Masaaki Kodama ◽  
Yoshiyuki Tsukamoto ◽  
Tadayoshi Okimoto ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Eradication Therapy ◽  
Basal Area ◽  
Immunofluorescent Staining ◽  
Upper Gastrointestinal Endoscopy ◽  
H Pylori ◽  
The Relationship

Abstract Background Although eradication therapy for chronic Helicobacter pylori reduces the risk of gastric cancer (GC), its effectiveness is incomplete. Therefore, it is critically important to identify those patients who remain at high risk after H. pylori eradication therapy. Accumulation of protein methylation is strongly implicated in cancer, and a recent study showed that dimethylation of eEF1A lysine 55 (eEF1AK55me2) promotes carcinogenesis in vivo. We aimed to investigate the relationship between eEF1A dimethylation and H. pylori status in gastric mucosa and to reveal potential downstream molecules of eEF1A dimethylation in H. pylori-eradicated mucosa. Methods Records of 115 patients (11 H. pylori-negative, 29 H. pylori-positive, 75 post-eradication patients) who underwent upper gastrointestinal endoscopy were retrospectively reviewed. The eEF1A dimethyl level was evaluated in each functional cell type of gastric mucosa by immunofluorescent staining. We also investigated the relationship between eEF1AK55me2 downregulation by CRISPR/Cas9-mediated deletion of Mettl13, which is known as a dimethyltransferase of eEF1AK55me2. Results The level of eEF1A dimethylation significantly increased in the surface and basal areas of H. pylori-positive mucosa compared with -negative mucosa (surface, p=0.0031; basal, p<0.0001). The eEF1A dimethyl levels in the surface area were significantly reduced by eradication therapy (p=0.005), but those in the basal area were maintained even after eradication therapy. Multivariate analysis revealed that high dimethylation of eEF1A in the basal area of the mucosa was the independent factor related to GC incidence (odds ratio=3.6611, 95% confidence interval=1.0350–12.949, p=0.0441). We also showed the relationship between eEF1A dimethylation and expressions of reprogramming factors Oct4 and Nanog by immunohistochemistry and in vitro genome editing experiments. Conclusions The results indicated that H. pylori infection potently induced eEF1A dimethylation in gastric mucosa. The accumulation of dimethyl-eEF1A in the basal area of the mucosa might contribute to GC risk via regulation of reprograming factors in H. pylori-eradicated gastric mucosa.

scholarly journals Helicobacter pylori Eradication Therapy - Recent Trend in Research

2020 ◽  
Vol 20 (3) ◽  
pp. 210-217
Author(s):  
Heung Up Kim
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Antibiotic Resistance ◽  
Gastric Mucosa ◽  
Drug Exposure ◽  
Eradication Therapy ◽  
Dual Therapy ◽  
Resistance Rate ◽  
H Pylori ◽  
Selection Of

It is well known that <i>Helicobacter pylori (H. pylori)</i> can cause peptic ulcer, mucosa-associated lymphoid tissue lymphoma, atrophic gastritis, intestinal metaplasia, and ultimately, gastric cancer. Various studies have proven that <i>H. pylori</i>, which attaches to the gastric mucosa, is the cause of gastric cancer and can be eradicated using appropriate antibiotics. Since 2013, Japan has been carrying out national-led eradication treatment of <i>H. pylori</i> for the whole population. However, as drug exposure increases, the resistance rate to some antibiotics increases, and the pattern of antibiotic resistance varies from region to region. Therefore, the development of individualized antimicrobial therapies has become important since antibiotic resistance to <i>H. pylori</i> eradication is a problem worldwide. To help overcome this, remedies such as selection of antibiotics through susceptibility testing, selection of empirical treatment combinations appropriate for the region, dual therapy with high doses of amoxicillin, and the use of rifabutin or sitafloxacin with low antibiotic resistance have been studied. Potassium-competitive acid blocker has been reported to be more potent in inhibiting acid secretion than proton pump inhibitor, and its role in <i>H. pylori</i> eradication is expected. Drug formulations and regimens that are easy to take are being developed to increase compliance. New treatments such as spraying antibiotics directly to the gastric mucosa are being developed and studied.

scholarly journals Amoxicillin secretion by gastric mucosa in Chernobyl nuclear power plant accident recovery workers with atrophic and nonatrophic gastritis undergoing eradication therapy

2020 ◽  
pp. 36-42
Author(s):  
A. O. Sablina ◽  
O. A. Sablin ◽  
S. S. Aleksanin ◽  
G. G. Rodionov ◽  
I. I. Shantyr' ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Power Plant ◽  
Nuclear Power Plant ◽  
Gastric Mucosa ◽  
Gastric Secretion ◽  
Nuclear Power ◽  
Eradication Therapy ◽  
Chernobyl Nuclear Power Plant ◽  
Normal Gastric Mucosa ◽  
H Pylori

Relevance. Today gastric cancer is still one of the oncologic diseases most often leading to death. H. pylori eradication reduces risk of gastric cancer, but its efficacy depends on gastric mucosa state. Atrophy of gastric mucosa is more common in Chernobyl nuclear power plant (CNPP) accident recovery workers than in patients who have not been involved in CNPP accident recovery works. It seems especially important to investigate the features of antibiotics transport to H. pylori colonization area in this contingent.Intention – to determine the features of amoxicillin secretion by gastric mucosa in CNPP accident recovery workers with atrophic and nonatrophic gastritis undergoing H. pylori eradication.Methodology. 65 CNPP accident recovery workers were divided into groups depending on state of gastric mucosa according to endoscopic and histological examination, immunosorbent assay of pepsinogens I and II and gastrin-17 basal serum levels. On the first day of eradication therapy, gastric secretion samples were obtained via nasogastric probe 30, 60, 120, 180 and 240 minutes after oral amoxicillin administration. Drug concentrations in gastric secretion were assessed via liquid chromatography-mass spectrometry.Results and discussion. Amoxicillin concentrations in gastric secretion samples were lower (р < 0.01) in patients with atrophic antral gastritis than in patients with normal gastric mucosa and atrophic fundal gastritis. Patients with fundal atrophy were characterized by lower amoxicillin concentrations 30 and 60 (p = 0.02) minutes after drug intake than in patients with normal gastric mucosa, and higher concentration in the 120th (p < 0.01) and 180th (p = 0.02) minute than in patients with antral atrophy. Amoxicillin concentrations in patients with antral atrophy were lower (p < 0.01) than in non-atrophy group in the 30th, 60th and 120th minute. In the 240th minute, amoxicillin concentrations in patients with fundal atrophy exceeded concentrations in both other groups (p < 0.01). Amoxicillin concentration peak was registered in patients with fundal and antral atrophy in the 180th minute, in patients without atrophy – from the 30th to 120th minute.Conclusion. Atrophy of gastric mucosa is characterized by decreased transport of orally administered amoxicillin from bloodstream to gastric lumen. Depending on gastric mucosa state, amoxicillin concentrations in gastric secretion should be evaluated at different time points after drug administration: in patients with atrophic gastritis – in the 180th minute, in patients without atrophy – in the 120th minute. While predicting the efficacy and choosing H. pylori eradication regimen, morphological and functional state of gastric mucosa should be taken into account.

scholarly journals Biofilm Formation byHelicobacter pyloriand Its Involvement for Antibiotic Resistance

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Hideo Yonezawa ◽  
Takako Osaki ◽  
Shigeru Kamiya
Keyword(s):  
Drinking Water ◽  
Antibiotic Resistance ◽  
Gastric Mucosa ◽  
Distribution System ◽  
Biofilm Formation ◽  
Eradication Therapy ◽  
Human Gastric Mucosa ◽  
Successful Infection ◽  
H Pylori

Bacterial biofilms are communities of microorganisms attached to a surface. Biofilm formation is critical not only for environmental survival but also for successful infection.Helicobacter pyloriis one of the most common causes of bacterial infection in humans. Some studies demonstrated that this microorganism has biofilm forming ability in the environment and on human gastric mucosa epithelium as well as onin vitroabiotic surfaces. In the environment,H. pyloricould be embedded in drinking water biofilms through water distribution system in developed and developing countries so that the drinking water may serve as a reservoir forH. pyloriinfection. In the human stomach,H. pyloriforms biofilms on the surface of gastric mucosa, suggesting one possible explanation for eradication therapy failure. Finally, based on the results ofin vitroanalyses,H. pyloribiofilm formation can decrease susceptibility to antibiotics andH. pyloriantibiotic resistance mutations are more frequently generated in biofilms than in planktonic cells. These observations indicated thatH. pyloribiofilm formation may play an important role in preventing and controllingH. pyloriinfections. Therefore, investigation ofH. pyloribiofilm formation could be effective in elucidating the detailed mechanisms of infection and colonization by this microorganism.

scholarly journals Early clinical and pathophysiological manifestations of gastric cancer at the outpatient clinic stage (The “RADIUS” study)

2020 ◽  
pp. 62-68
Author(s):  
N. N. Dekhnich ◽  
L. B. Lazebnik ◽  
A. A. Tryapyshko ◽  
N. D. Elistratov ◽  
E. D. Rzhevtseva ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Gastric Mucosa ◽  
Primary Care Physicians ◽  
Epigastric Pain ◽  
Demographic Data ◽  
Precancerous Lesion ◽  
Eradication Therapy ◽  
Warning Signs ◽  
Previous Diagnosis ◽  
H Pylori

Objective. To study the early clinical and pathophysiological manifestations of gastric cancer in the outpatient phasefor early diagnosis disease.Methods. A total of 300 outpatient cards of patients treated in Smolensk Oncology Hospital with gastric cancer were analyzed during 2016-2019. Data collection included filling out a questionnaire consisting of 32 questions aimed at clarifying demographic data, diagnosing the symptoms of the disease and their duration, identifying the warning signs, precancerous lesion of the gastric mucosa, previous diagnosis and treatment of H. pylori. The study included patients with gastric cancer aged 31 to 88 years. The mean age of patients was 65.12±9.92 years, the median age was 65.5 years. Among 300 patients, 153 (51%) were male and 147 (49%) were female.Results. 2.7% (n=8) of diagnosed patients account for young people. 32.7% (n=98) of patients were diagnosed with the stage II cancer, 32.3% (n=97) — with the stage III cancer. The most common symptoms of the disease were epigastric pain — 57% (n=171), dysphagia — 19.3% (n=58), nausea — 15% (n=45), unmotivated weight loss — 12% (n=36) and epigastric burning — 7% (n=21). These symptoms bothered patients up to 6 months in 32.7% (n=98) of cases. Biochemical blood tests (80%, n=192/240), accelerated ESR (76%, n=183/241), decreased hemoglobin (69%, n=178/258), and leukocytosis (48%, n=120/248) were identified as the most common “warning” signs. 24.7% (n=74) of patients had atrophic gastritis preceded the development of gastric cancer, 24% (n=72) — gastric ulcer, 12% (n=36) — polyps of the stomach. The previous diagnostics of H. pylori was carried out only in 1.3% (n=4) of patients.Conclusions. If a patient, including a young patient, has epigastric pain, primary care physicians should recommend esophagogastroduodenoscopy with biopsies to determine precancerous changes in the gastric mucosa and the presence of H. pylori, followed by eradication therapy.

Role of vitamin C in gastric cancer

2018 ◽  
Vol 01 (1) ◽  
Author(s):  
Takalkar U Vidyadhar
Keyword(s):  
Gastric Cancer ◽  
Vitamin C ◽  
Gastric Juice ◽  
Oxidative Dna Damage ◽  
Preventive Measure ◽  
Dietary Factors ◽  
Preventive Strategy ◽  
H Pylori

Gastric cancer is a multifactorial disease with complex interplay of environmental and genetic factors. Helicobacter pylori (H. pylori) infestation has been identified as the most important etiological agent in the pathogenesis of gastric cancer. Also, the role of dietary factors that is low consumption of fruits and vegetables have been found to be associated with gastric cancer. Among the dietary factors, antioxidants especially vitamin C has been found to confer the strongest protection against gastric cancer. Its anti-proliferative and pro-apoptotic action has been suggested in vitro. Because of its antioxidant activity, it protects cells against oxidative DNA damage caused by toxic effects of reactive oxygen species. It also inhibits production of carcinogenic N-nitroso compound in the stomach. The person with H. pylori infection has low levels of vitamin C in their gastric juice and levels of vitamin C normalizes on eradication of H. pylori. Vitamin C levels are high in gastric mucosa and gastric juice, sometimes more than that of in plasma. But gastric pathological conditions cause lowered secretion of vitamin C into gastric juice. Effect of H. pylori on vitamin C in gastric juice is reversible and on eradication of H. pylori, it returns to normal level. Hence, eradication of H. pylori and chemoprevention with antioxidant supplementation will be an effective preventive strategy to reduce the incidence of gastric cancer and related mortality. Vitamin C and gastric cancer is an area of potential interest for researchers as a preventive measure. Keywords: Vitamin C, H. pylori, gastric cancer.

scholarly journals Helicobacter pylori Virulence Factors—Mechanisms of Bacterial Pathogenicity in the Gastric Microenvironment

Cells ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 27
Author(s):  
Jacek Baj ◽  
Alicja Forma ◽  
Monika Sitarz ◽  
Piero Portincasa ◽  
Gabriella Garruti ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Virulence Factors ◽  
Premalignant Lesions ◽  
Bacterial Pathogenicity ◽  
Current State ◽  
Genetic And Environmental Factors ◽  
H Pylori ◽  
Stimulation Of

Gastric cancer constitutes one of the most prevalent malignancies in both sexes; it is currently the fourth major cause of cancer-related deaths worldwide. The pathogenesis of gastric cancer is associated with the interaction between genetic and environmental factors, among which infection by Helicobacter pylori (H. pylori) is of major importance. The invasion, survival, colonization, and stimulation of further inflammation within the gastric mucosa are possible due to several evasive mechanisms induced by the virulence factors that are expressed by the bacterium. The knowledge concerning the mechanisms of H. pylori pathogenicity is crucial to ameliorate eradication strategies preventing the possible induction of carcinogenesis. This review highlights the current state of knowledge and the most recent findings regarding H. pylori virulence factors and their relationship with gastric premalignant lesions and further carcinogenesis.

Prevalence of Helicobacter pylori infection among blood donors in Saxony-Anhalt, Germany – a region at intermediate risk for gastric cancer

2017 ◽  
Vol 55 (07) ◽  
pp. 653-656 ◽  
Author(s):  
Caspar Franck ◽  
Armin Hoffmann ◽  
Alexander Link ◽  
Christian Schulz ◽  
Kerstin Wuttig ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Blood Donors ◽  
Eradication Therapy ◽  
Surrogate Marker ◽  
University Hospital ◽  
Study Cohort ◽  
Emergency Ward ◽  
Age Related ◽  
H Pylori

Abstract Background In the federal state of Saxony-Anhalt, gastric cancer (GC) incidence ranks among the highest in Germany. Helicobacter pylori prevalence is a surrogate marker for GC risk in a given population. In 2010 we reported an H. pylori seroprevalence of 44.4 % in patients at the emergency ward of the University Hospital of Magdeburg, the capital of Saxony-Anhalt. Our aim is to update these findings in a cohort of healthy blood donors from the same region. Materials and methods The sera of 516 consecutive blood donors (40.1 ± 14.1 years; 286 males and 230 females) were tested for antibodies against H. pylori and CagA. Data on demographics and previous H. pylori eradication therapy were obtained by means of a structured questionnaire. Blood donors with positive serology for H. pylori or CagA and/or history of eradication therapy were classified as H. pylori-positive. Results Overall, 28.9 % of the study cohort were H. pylori-positive. The prevalence was higher in older generations (9 % in 18 – 20 years up to 47 % in 61 – 70 years). In 44.4 % of H. pylori IgG-positive donors, CagA serology was also positive. This proportion was not age-dependent. Study participants with siblings were by trend more often H. pylori-positive (p = 0.066). Conclusion Compared to our previous study in patients at the emergency ward, we found by trend lower age-related H. pylori prevalence rates. In our cohort of healthy blood donors, we confirmed a lower H. pylori prevalence in younger generations.

scholarly journals Differential Normalization of Mucosal Interleukin-8 and Interleukin-6 Activity after Helicobacter pyloriEradication

1998 ◽  
Vol 66 (10) ◽  
pp. 4742-4747 ◽  
Author(s):  
Takafumi Ando ◽  
Kazuo Kusugami ◽  
Masahiro Ohsuga ◽  
Kenji Ina ◽  
Masataka Shinoda ◽  
...  
Keyword(s):  
Mononuclear Cells ◽  
Eradication Therapy ◽  
Interleukin 8 ◽  
Biopsy Specimens ◽  
Mucosal Tissues ◽  
H Pylori ◽  
Triple Treatment

ABSTRACT There is differential resolution of mucosal infiltration with neutrophils and mononuclear cells following successfulHelicobacter pylori eradication. We investigated the effects of H. pylori eradication on mucosal interleukin-8 (IL-8) and IL-6 activity in relation to the resolution of H. pylori-associated gastritis. Eighty-one duodenal ulcer patients with H. pyloriinfection received dual- or triple-treatment eradication therapy, and mucosal biopsy specimens obtained at the initial and follow-up endoscopic examinations were cultured in vitro for 24 h. The levels of IL-8 and IL-6 were measured by enzyme-linked immunosorbent assays. In the 42 patients in whomH. pylori eradication failed, there was little change in the numbers of neutrophils and mononuclear cells infiltrating the mucosa and in IL-8 and IL-6 activity. In the 39 patients in whom H. pylori was eradicated, there was normalization both in the numbers of infiltrating neutrophils and in mucosal IL-8 activity, which was evident within 1 month following therapy. In contrast, there was a gradual resolution of mononuclear cell infiltration over a 6-month period, accompanied by a gradual normalization in IL-6 levels. Addition of H. pylori to cultures of mucosal tissues induced a significant increase in IL-8 activity in both uninfected control subjects and patients from whom H. pylori was eradicated. However, this introduction yielded a significant increase in IL-6 activity only in the latter group. This study indicates a dichotomy in the changes of mucosal IL-8 and IL-6 activity afterH. pylori eradication. The rapid normalization of IL-8 after H. pylori eradication and the ability of H. pylori cells to stimulate IL-8 in control tissues indicate that IL-8 induction is a part of the innate (nonimmune) responses to this organism. In contrast, the results of experiments analyzing IL-6 activity in cultured mucosal tissues suggest that the gradual resolution of mucosal IL-6 activity and mononuclear infiltration after successful eradication observed in vivo may reflect gradually diminishing residual immune responses against H. pylori.

scholarly journals In VitroInhibition ofHelicobacter pyloriGrowth by Redox Cycling Phenylaminojuglones

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Julio Benites ◽  
Héctor Toledo ◽  
Felipe Salas ◽  
Angélica Guerrero ◽  
David Rios ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Antibacterial Activity ◽  
Active Compound ◽  
Metabolic Pathways ◽  
Growth Inhibitor ◽  
Growth Inhibitors ◽  
Design Synthesis ◽  
H Pylori

Infection byHelicobacter pyloriincreases 10 times the risk of developing gastric cancer. Juglone, a natural occurring 1,4-naphthoquinone, preventsH. pylorigrowth by interfering with some of its critical metabolic pathways. Here, we report the design, synthesis, andin vitroevaluation of a series of juglone derivatives, namely, 2/3-phenylaminojuglones, as potentialH. pylorigrowth inhibitors. Results show that 5 out of 12 phenylaminojuglones (at 1.5 μg/mL) were 1.5–2.2-fold more active than juglone. Interestingly, most of the phenylaminojuglones (10 out of 12) were 1.1–2.8 fold more active than metronidazole, a knownH. pylorigrowth inhibitor. The most active compound, namely, 2-((3,4,5-trimethoxyphenyl)amino)-5-hydroxynaphthalene-1,4-dione 7, showed significant higher halo of growth inhibitions (HGI = 32.25 mm) to that of juglone and metronidazole (HGI = 14.50 and 11.67 mm). Structural activity relationships of the series suggest that the nature and location of the nitrogen substituents in the juglone scaffold, likely due in part to their redox potential, may influence the antibacterial activity of the series.

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