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Efficacy of Vonoprazan for Helicobacter pylori Eradication.
Kiyotoki, S, Nishikawa, J, Sakaida, I
Internal medicine (Tokyo, Japan). 2020;(2):153-161
Abstract
Helicobacter pylori can infect the gastric mucosa and cause chronic inflammation, resulting in various diseases, including gastric cancer. Eradication of H. pylori in all infected subjects is recommended; however, the number of H. pylori strains with antibiotic resistance has increased, and the eradication rate has decreased. Vonoprazan, a potassium-competitive acid blocker, produces a stronger acid-inhibitory effect than proton pump inhibitors (PPIs). The H. pylori eradication rate with vonoprazan was found to be higher than that with PPIs. The H. pylori eradication rate with vonoprazan-based triple therapy (vonoprazan, amoxicillin, and clarithromycin) was approximately 90% and had an incidence of adverse events similar to that of PPIs. We review the current situation of H. pylori eradication in Japan, the first country in which vonoprazan was made available.
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ATP Analogues for Structural Investigations: Case Studies of a DnaB Helicase and an ABC Transporter.
Lacabanne, D, Wiegand, T, Wili, N, Kozlova, MI, Cadalbert, R, Klose, D, Mulkidjanian, AY, Meier, BH, Böckmann, A
Molecules (Basel, Switzerland). 2020;(22)
Abstract
Nucleoside triphosphates (NTPs) are used as chemical energy source in a variety of cell systems. Structural snapshots along the NTP hydrolysis reaction coordinate are typically obtained by adding stable, nonhydrolyzable adenosine triphosphate (ATP) -analogues to the proteins, with the goal to arrest a state that mimics as closely as possible a physiologically relevant state, e.g., the pre-hydrolytic, transition and post-hydrolytic states. We here present the lessons learned on two distinct ATPases on the best use and unexpected pitfalls observed for different analogues. The proteins investigated are the bacterial DnaB helicase from Helicobacter pylori and the multidrug ATP binding cassette (ABC) transporter BmrA from Bacillus subtilis, both belonging to the same division of P-loop fold NTPases. We review the magnetic-resonance strategies which can be of use to probe the binding of the ATP-mimics, and present carbon-13, phosphorus-31, and vanadium-51 solid-state nuclear magnetic resonance (NMR) spectra of the proteins or the bound molecules to unravel conformational and dynamic changes upon binding of the ATP-mimics. Electron paramagnetic resonance (EPR), and in particular W-band electron-electron double resonance (ELDOR)-detected NMR, is of complementary use to assess binding of vanadate. We discuss which analogues best mimic the different hydrolysis states for the DnaB helicase and the ABC transporter BmrA. These might be relevant also to structural and functional studies of other NTPases.
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Gastric Parietal Cell Physiology and Helicobacter pylori-Induced Disease.
Yao, X, Smolka, AJ
Gastroenterology. 2019;(8):2158-2173
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Abstract
Acidification of the gastric lumen poses a barrier to transit of potentially pathogenic bacteria and enables activation of pepsin to complement nutrient proteolysis initiated by salivary proteases. Histamine-induced activation of the PKA signaling pathway in gastric corpus parietal cells causes insertion of proton pumps into their apical plasma membranes. Parietal cell secretion and homeostasis are regulated by signaling pathways that control cytoskeletal changes required for apical membrane remodeling and organelle and proton pump activities. Helicobacter pylori colonization of human gastric mucosa affects gastric epithelial cell plasticity and homeostasis, promoting epithelial progression to neoplasia. By intervening in proton pump expression, H pylori regulates the abundance and diversity of microbiota that populate the intestinal lumen. We review stimulation-secretion coupling and renewal mechanisms in parietal cells and the mechanisms by which H pylori toxins and effectors alter cell secretory pathways (constitutive and regulated) and organelles to establish and maintain their inter- and intracellular niches. Studies of bacterial toxins and their effector proteins have provided insights into parietal cell physiology and the mechanisms by which pathogens gain control of cell activities, increasing our understanding of gastrointestinal physiology, microbial infectious disease, and immunology.
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H. pylori infection and extra-gastroduodenal diseases.
Tsay, FW, Hsu, PI
Journal of biomedical science. 2018;(1):65
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Abstract
Helicobacter pylori infection is the principal cause of peptic ulcer disease, gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue lymphoma. Recent studies have shown that it may interfere with many biological processes and determine or influence the occurrence of many diseases outside the stomach. Currently, the role of H. pylori in idiopathic thrombocytopenic purpura and iron deficiency anemia is well documented. Emerging evidence suggests that it may also contribute to vitamin B12 deficiency, insulin resistance, metabolic syndrome, diabetes mellitus and non-alcoholic liver disease. Additionally, it may increase the risk of acute coronary syndrome, cerebrovascular disease, neurodegenerative disease and other miscellaneous disorders. Different pathogenic mechanisms have been hypothesized, including the occurrence of molecular mimicry and the induction of a low-grade inflammation. This review summarizes the results of the most relevant studies on the extra-gastroduodenal manifestations of H. pylori infection.
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Helicobacter pylori infection: old and new.
Diaconu, S, Predescu, A, Moldoveanu, A, Pop, CS, Fierbințeanu-Braticevici, C
Journal of medicine and life. 2017;(2):112-117
Abstract
Helicobacter pylori is a spiral-shaped bacterium that grows in the digestive tract and may be present in more than half of the world's population. The clinical features of Helicobacter pylori range from asymptomatic gastritis to gastrointestinal malignancy. Mucosa-associated lymphoid tissue (MALT) lymphoma is a low-grade B-cell marginal zone lymphoma and Helicobacter pylori has been detected in more than 75% of the patients with MALT lymphoma. Many tests for the detection of Helicobacter pylori are available, including antibody tests, urea breath tests, stool antigen tests and endoscopic biopsies. The eradication of Helicobacter pylori usually prevents the return of ulcers and ulcer complications even after appropriate medications such as PPIs are stopped. The eradication of Helicobacter pylori is important in the treatment of the rare condition of the stomach known as MALT lymphoma. The treatment of Helicobacter pylori to prevent stomach cancer is controversial. Confirmation of eradication is recommended in associated ulcers, persistent dyspepsia despite a test-and-treat approach, MALT lymphoma, and previous treatment for early-stage gastric cancer. The urea breath test and stool antigen test can be used to confirm the eradication and should be performed at least 4 weeks after the completion of therapy. Several diseases have been reported to be associated with Helicobacter pylori infection, including hematologic diseases, such as ITP, idiopathic iron deficiency anemia and vitamin B12 deficiency. There is a positive trend in the association between Helicobacter pylori infection and neurodegenerative disorders and new data showed a reduced risk of death due to stroke and lung cancer but an increased risk of preeclampsia in infected women, which requires further investigations.
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Helicobacter pylori Infection and Dietary Factors Act Synergistically to Promote Gastric Cancer.
Raei, N, Behrouz, B, Zahri, S, Latifi-Navid, S
Asian Pacific journal of cancer prevention : APJCP. 2016;(3):917-21
Abstract
However, the incidence of gastric cancer (GC) has been decreased in past decades; GC is the second cause of cancer related death in the world. Evidence has illustrated that several factors including Helicobacter pylori (H. pylori) infection, host genetics, and environmental factors (smoking and particularly diet) may play a crucial role in gastric carcinogenesis. It has been demonstrated that high consumption of fresh fruits, vegetables, high level of selenium and zinc in drinking water, sufficient iron, and cholesterol protect against GC, while; smoked , pickled, and preserved foods in salt, and nitrites increase the risk of GC. Epidemiological studies have also proved that H. pylori infection and a high salt diet could independently induce atrophic gastritis and intestinal metaplasia. Recently, studies have been demonstrated that dietary factors directly influence H. pylori virulence. The use of appropriate diet could reduce levels of H. pylori colonization or virulence and prevent or delay development of peptic ulcers or gastric carcinoma. This is attractive from a number of perspectives including those of cost, treatment tolerability, and cultural acceptability. This review will describe new insights into the pathogenesis of H. pylori in relation to environmental factors, especially dietary, not only to find the developed means for preventing and treating GC, but also for understanding the role of chronic inflammation in the development of other malignancies.
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At the bedside: Helicobacter pylori, dysregulated host responses, DNA damage, and gastric cancer.
Dalal, RS, Moss, SF
Journal of leukocyte biology. 2014;(2):213-24
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Abstract
Clinical trials performed in populations at high GC risk have demonstrated that eradication of Helicobacter pylori from the stomach with a course of combination antimicrobials helps prevent gastric carcinogenesis when they are administered before precancerous lesions have yet developed. In this review, we consider the insights into H. pylori-associated gastric carcinogenesis that have been gained from these and many other clinical studies in the field to highlight priority areas for basic research and clinical investigation. Among these are defining the magnitude of the risk reduction that may be achieved in clinical practice and at a population level by H. pylori eradication and investigating when, during the slow multistep progression to GC, intervention will be of the most benefit. Additional strategies to prevent GC induced by H. pylori, including chemoprevention, dietary modification, and close endoscopic surveillance, may also have value in augmenting the risk reduction. Why only a small subpopulation of those infected by H. pylori go on to develop GC may be partially explained by genetic susceptibility related to SNPs in several genes regulating the intensity of the gastric inflammatory response to H. pylori. Investigation of the basic mechanisms underlying the promotion of GC by H. pylori and the associated inflammatory response will likely continue to improve clinical strategies for the prevention of one of the most common causes of cancer death globally. See related review, At the Bench: H. pylori, dysregulated host responses, DNA damage, and gastric cancer.
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At the Bench: Helicobacter pylori, dysregulated host responses, DNA damage, and gastric cancer.
Hardbower, DM, Peek, RM, Wilson, KT
Journal of leukocyte biology. 2014;(2):201-12
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Abstract
Helicobacter pylori infection is the strongest known risk factor for the development of gastric cancer. Given that ∼50% of the global population is infected with this pathogen, there is great impetus to elucidate underlying causes that mediate progression from infection to cancer. Recent evidence suggests that H. pylori-induced chronic inflammation and oxidative stress create an environment conducive to DNA damage and tissue injury. DNA damage leads to genetic instability and eventually, neoplastic transformation. Pathogen-encoded virulence factors induce a robust but futile immune response and alter host pathways that lower the threshold for carcinogenesis, including DNA damage repair, polyamine synthesis and catabolism, antioxidant responses, and cytokine production. Collectively, such dysregulation creates a protumorigenic microenvironment within the stomach. This review seeks to address each of these aspects of H. pylori infection and to call attention to areas of particular interest within this field of research. This review also seeks to prioritize areas of translational research related to H. pylori-induced gastric cancer based on insights garnered from basic research in this field. See related review by Dalal and Moss, At the Bedside: H. pylori, dysregulated host responses, DNA damage, and gastric cancer.
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Helicobacter pylori infection: new pathogenetic and clinical aspects.
Hagymási, K, Tulassay, Z
World journal of gastroenterology. 2014;(21):6386-99
Abstract
Helicobacter pylori (H. pylori) infects more than half of the world's human population, but only 1% to 3% of infected people consequently develop gastric adenocarcinomas. The clinical outcome of the infection is determined by host genetic predisposition, bacterial virulence factors, and environmental factors. The association between H. pylori infection and chronic active gastritis, peptic ulcer disease, gastric cell carcinoma, and B cell mucosa-associated lymphoid tissue lymphoma has been well established. With the exception of unexplained iron deficiency anemia and idiopathic thrombocytopenic purpura, H. pylori infection has no proven role in extraintestinal diseases. On the other hand, there is data showing that H. pylori infection could be beneficial for some human diseases. The unpredictability of the long-term consequences of H. pylori infection and the economic challenge in eradicating it is why identification of high-risk individuals is crucial.
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Probiotics for the treatment of Helicobacter pylori infection in children.
Pacifico, L, Osborn, JF, Bonci, E, Romaggioli, S, Baldini, R, Chiesa, C
World journal of gastroenterology. 2014;(3):673-83
Abstract
The combination of a proton pump inhibitor and two antibiotics (clarithromycin plus amoxicillin or metronidazole) has been the recommended first-line therapy since the first guidelines for Helicobacter pylori (H. pylori) infection in children were published. In recent years, the success of eradication therapies has declined, in part due to the development of H. pylori resistant strains. Alternative anti-H. pylori treatments are currently becoming more popular than the traditional eradication methods. Components that may be used either as a monotherapy or, in combination with antimicrobials, resulting in a more effective anti-H. pylori therapy have been investigated in depth by several researchers. One of the potential therapies is probiotic cultures; promising results have been observed in initial studies with numerous probiotic strains. Nevertheless, many questions remain unanswered. In this article, we comprehensively review the possible mechanisms of action of probiotics on H. pylori infection, and present the results of published studies using probiotics as possible agents to control H. pylori infection in children. The effect of the addition of probiotics to the standard H. pylori eradication therapy for the prevention of antibiotic associated side-effects is also discussed.