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Sakaguchi, Takuki, Takaaki Sugihara, Ken Ohnita, Daisuke Fukuda, Tetsuro Honda, Ryohei Ogihara, Hiroki Kurumi, Kazuo Yashima, and Hajime Isomoto. "Pyloric Incompetence Associated with Helicobactor pylori Infection and Correlated to the Severity of Atrophic Gastritis." Diagnostics 12, no. 3 (February 23, 2022): 572. http://dx.doi.org/10.3390/diagnostics12030572.
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Duodenogastric reflux (DGR) causes bile reflux gastritis (BRG) and may develop into gastric cancer. DGR is classified as primary in non-operated stomachs or secondary to surgical intervention. Primary DGR and Helicobacter pylori (H. pylori) infection are reportedly related. However, the mechanism is not fully understood. This study aimed to elucidate the relationship between H. pylori infection and pyloric incompetence in a non-operated stomach. A total of 502 non-operated participants who underwent an upper intestinal endoscopy were prospectively enrolled. Endoscopic findings (EAC, endoscopic atrophy classification; nodular gastritis; xanthoma; fundic gland polyp; and incompetence of pylorus), sex, age, gastrin, pepsinogen (PG) I and PG II levels were evaluated. PG I/PG II ratio, anti-H. pylori-Ab positivity, and atrophic gastritis status were significantly different between the normal and incompetent pylori (p = 0.043, <0.001, and 0.001, respectively). Open-type atrophic gastritis was significantly higher in the incompetent pylori. Incompetence of the pylorus and EAC were moderately correlated (Cramer’s V = 0.25). Multivariate analysis revealed that the presence of anti-H. pylori-Ab was the only independent factor associated with the incompetence of the pylorus, with an adjusted odds ratio of 2.70 (95% CI: 1.47–4.94, p = 0.001). In conclusion, pyloric incompetence was associated with H. pylori infection and moderately correlated to the severity of atrophic gastritis in non-operated stomachs.
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Chiba, N., A. Matisko, P. Sinclair, and ABR Thomson. "Helicobacter pylori: From Bench to Bedside." Canadian Journal of Gastroenterology 11, no. 7 (1997): 589–96. http://dx.doi.org/10.1155/1997/975469.
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With the exponential increase in research in the field ofHelicobacter pyloria paradigm shift has occurred. It is now recognized thatH pyloriis a chronic infection of the stomach causing inflammation. Some patients remain asymptomatic, while others may develop dyspepsia, duodenal or gastric ulcer, gastric cancer or a mucosa-associated lymphoid tissue lymphoma. However, the role ofH pyloriin contributing to nonulcer dyspepsia or nonsteroidal anti-inflammatory drug gastropathy remains controversial. An effective vaccine againstH pyloriis years away. Major interest has focused on the questions "who should be investigated and therefore treated" and "what is the latest gold standard for eradication ofH pylori"? In Europe, guidelines have been developed to help the practitioner answer these important questions. Canadian guidelines will soon be available. For persons with known peptic ulcer disease there should be unequivocal acceptance that the good clinical practice of eradicatingH pyloriwill result in substantial savings in health care expenses. The original 'classical triple therapy' (bismuth, metronidazole and tetracycline [BMT]) has now been surpassed by the combination of a proton pump inhibitor (PPI) plus two antibiotics (metronidazole plus clarithromycin; amoxicillin plus clarithromycin; or amoxicillin plus metronidazole), each given twice a day for one week. In Canada, the regimen of omeprazole plus one antibiotic (amoxicillin or clarithromycin) was approved recently but gives an eradication rate that is lower than the current target of 90%. According to the European (Mäastricht) recommendations, if a single treatment attempt with PPI plus two antibiotics fails, PPI plus BMT is recommended.
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Garcés-Duran, R., S. Kindt, K. Kotilea, S. François, G. Rasschaert, A. Smet, B. Hauser, et al. "Belgian consensus for Helicobacter pylori management 2023." Acta Gastro Enterologica Belgica 86, no. 1 (March 2023): 74–91. http://dx.doi.org/10.51821/86.1.11327.
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Helicobacter pylori (H. pylori) infection causes chronic gastritis, peptic ulcers and gastric cancer. Although H. pylori prevalence is decreasing worldwide, regional variations exist in Europe, with the lowest infection prevalence in Northern Europe, and the highest in Eastern and Southern Europe (1). Changes in the treatment recommendations and the increasing available evidence have justified the implementation of new recommendations since last Belgian consensus in 1998 (2). Several non-H. pylori Helicobacter species (NH.PYLORI-H), colonizing the stomach of domestic animals, also have the ability to cause gastric disease in humans, although to a lesser extent. These zoonotic NH. PYLORIH are not the subject of the current recommendations.
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Asonuma, Sho, Akira Imatani, Naoki Asano, Tomoyuki Oikawa, Hidetomo Konishi, Katsunori Iijima, Tomoyuki Koike, Shuichi Ohara, and Tooru Shimosegawa. "Helicobacter pylori induces gastric mucosal intestinal metaplasia through the inhibition of interleukin-4-mediated HMG box protein Sox2 expression." American Journal of Physiology-Gastrointestinal and Liver Physiology 297, no. 2 (August 2009): G312—G322. http://dx.doi.org/10.1152/ajpgi.00518.2007.
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Helicobacter pylori is a major cause of the transdifferentiation into intestinal metaplasia that may develop gastric cancer. However, the molecular pathogenesis of this transdifferentiation is poorly understood. A SRY-related HMG box protein Sox2 is an essential transcription factor of organ development in brain, lung, and stomach. Our aim of this study was to investigate the mechanism responsible for regulation of Sox2 in host Th1-dominant response to H. pylori. Sox2 protein was immunohistochemically expressed in both human oxyntic and pyloric glands with H. pylori infection, but not in intestinal metaplasia. Western immunoblotting of gastric epithelial cell lines showed that IL-4, a Th2-related cytokine, dose dependently enhanced Sox2 expression among H. pylori infection-mediated cytokines. Small changes of Sox2 expression were observed after each treatment with IFN-γ, IL-1β, or TNF-α. IL-4-mediated Sox2 induction was suppressed by the inhibition of STAT6 activation with STAT6 RNA interference, and electrophoretic mobility shift assay indicated that activation of the Sox2 promoter by IL-4 occurred through the action of STAT6. Furthermore, H. pylori and IFN-γ inhibited the phosphorylation of STAT6, resulting in the suppression of IL-4-mediated Sox2 expression. Immunohistochemical analyses showed significantly the suppressed STAT6 activity in H. pylori-infected human gastric mucosa. Additionally, downregulation of Sox2 by knockdown experiments led to intestinal phenotype with expressions of Cdx2 and MUC2. These results suggest that H. pylori and IFN-γ interfere with the differentiation into oxyntic and pyloric glands by the downregulation of Sox2 on IL-4/STAT6 signaling, which may contribute to the transdifferentiation into intestinal metaplasia.
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Hou, Yi-Ping, Yong-Ping Zhang, Yan-Feng Song, Chun-Min Zhu, Yin-Chun Wang, and Gui-Lin Xie. "Botulinum toxin type A inhibits rat pyloric myoelectrical activity and substance P release in vivo." Canadian Journal of Physiology and Pharmacology 85, no. 2 (February 2007): 209–14. http://dx.doi.org/10.1139/y07-018.
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The effect of botulinum toxin type A (BTX-A) on rat pyloric myoelectrical activity in vivo and the content and distribution of substance P (SP) in pylorus were investigated, respectively, with electromyography, radioimmunoassay, and immunohistochemistry. A pair of electrodes for recording pyloric myoelectrical activity and a guide cannula for drug injection were implanted into the pylorus. The changes of pyloric myoelectrical activity were recorded followed vehicle, 10, 20, and 40 U/kg body mass of BTX-A injection. Pyloric tissues were dissected for radioimmunoassay and immunohistochemistry after recording. The 3 dosages of BTX-A injections caused the reduction of slow wave of pyloric myoelectrical activity in amplitude but not in frequency and the diminishment of spike activity in amplitude and spike burst. The inhibitory effect of 20 U/kg BTX-A was significantly different from that of 10 U/kg (p < 0.05), but not from the effect of 40 U/kg administration (p > 0.05). After BTX-A intrasphincteric injection, SP content was reduced in the pylorus, and cell number of SP-immunoreactivity was decreased more in myenteric nerve plexus of circular muscle and in mucosa of pylori. In conclusion, BTX-A inhibits pyloric myoelectrical slow activity in amplitude and spike activity and weakens pyloric smooth muscle contractility depending on threshold of dose or concentration. BTX-A-induced inhibition of pyloric myoelectrical activity implies a mechanism of inhibiting SP release from the autonomic and enteric nervous terminals in the pylorus.
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Saler, Tayyibe, Şakir Özgür Keşkek, Sibel Kırk, Süleyman Ahbab, and Gülay Ortoğlu. "H. pyloriMay Not Be Associated with Iron Deficiency Anemia in Patients with Normal Gastrointestinal Tract Endoscopy Results." Advances in Hematology 2014 (2014): 1–4. http://dx.doi.org/10.1155/2014/375915.
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Background. The aim of this study was to investigate the association between iron deficiency anemia andH. pyloriin patients with normal gastrointestinal tract endoscopy results.Materials and Methods. A total of 117 male patients with normal gastrointestinal tract endoscopy results were included in this retrospective study. The study and control groups included 69 and 48 patients with and without iron deficiency anemia, respectively. The prevalence ofH. pylori, the number of RBCs, and the levels of HGB, HTC, MCV, iron, and ferritin were calculated and compared.Results. There was no statistically significant difference found between the groups according to the prevalence ofH. pylori(65.2% versus 64.6%,P=0.896). Additionally, the levels of RBCs, HGB, HTC, MCV, iron, and ferritin in the patients in the study group were lower than those in the control group (P<0.05). Finally, there was no association between iron deficiency anemia andH. pylori(OR 1.02, Cl 95% 0.47–2.22, andP=0.943).Conclusion.H. pyloriis not associated with iron deficiency anemia in male patients with normal gastrointestinal tract endoscopy results.
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Takatsuna, Masafumi, Rie Azumi, Takeshi Mizusawa, Hiroki Sato, Ken-Ichi Mizuno, Takashi Kato, Junji Yokoyama, Yoichi Ajioka, and Shuji Terai. "A case of Helicobacter pylori-negative early gastric adenocarcinoma with gastrointestinal phenotype." Endoscopy International Open 09, no. 06 (May 27, 2021): E863—E866. http://dx.doi.org/10.1055/a-1396-3854.
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AbstractA 40-year-old man with slightly depressed (0-IIc) type gastric cancer of the pyloric anterior gastric area underwent pre-operative screening for tetralogy of Fallot and endoscopic submucosal dissection (ESD) and was tested for Helicobacter pylori antigens and antibodies. Both tests were negative. He did not have a history of eradication. Pathological diagnosis of ESD showed a well-differentiated adenocarcinoma. The tumor was CD10-positive, MUC5AC-negative, and MUC6-confocal positive; it showed differentiation with gastrointestinal phenotype. Moreover, the tumor cells were lysozyme-positive, resembling Paneth cells. Mucosal glands exhibited intestinal metaplasia on the anal side of the tumor lesion. On the oral side of the tumor, metaplasia was non-existent, with normal pyloric glands present in the mucosal layer. The patient was not infected with H. pylori; however, intestinal metaplasia existed around the early gastric cancer. This suggested that the intestinal metaplasia occurred due to bile reflux, and the gastric neoplasia arose with the metaplasia without an H. pylori infection. This case may potentially help explain gastric cancer development in the absence of H. pylori infection.
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Kosai, Nik Ritza, Hardip Singh Gendeh, Abdul Rashid Norfaezan, Jamin Razman, Paul Anthony Sutton, and Srijit Das. "Prolapsing Gastric Polyp Causing Intermittent Gastric Outlet Obstruction." International Surgery 100, no. 6 (June 1, 2015): 1148–52. http://dx.doi.org/10.9738/intsurg-d-14-00205.1.
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Gastric polyps are often an incidental finding on upper gastrointestinal endoscopy, with an incidence up to 5%. The majority of gastric polyps are asymptomatic, occurring secondary to inflammation. Prior reviews discussed Helicobacter pylori (H pylori)–associated singular gastric polyposis; however, we present a rare and unusual case of recurrent multiple benign gastric polyposis post H pylori eradication resulting in intermittent gastric outlet obstruction. A 70-year-old independent male, Chinese in ethnicity, with a background of diabetes mellitus, hypertension, and a simple renal cyst presented with a combination of melena, anemia, and intermittent vomiting of partially digested food after meals. Initial gastroscopy was positive for H pylori; thus he was treated with H pylori eradication and proton pump inhibitors. Serial gastroscopy demonstrated multiple sessile gastric antral polyps, the largest measuring 4 cm. Histopathologic examination confirmed a benign hyperplastic lesion. Computed tomography identified a pyloric mass with absent surrounding infiltration or metastasis. A distal gastrectomy was performed, whereby multiple small pyloric polyps were found, the largest prolapsing into the pyloric opening, thus explaining the intermittent nature of gastric outlet obstruction. Such polyps often develop from gastric ulcers and, if left untreated, may undergo neoplasia to form malignant cells. A distal gastrectomy was an effective choice of treatment, taking into account the polyp size, quantity, and potential for malignancy as opposed to an endoscopic approach, which may not guarantee a complete removal of safer margins and depth. Therefore, surgical excision is favorable for multiple large gastric polyps with risk of malignancy.
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Öztekin, Merve, Birsen Yılmaz, Duygu Ağagündüz, and Raffaele Capasso. "Overview of Helicobacter pylori Infection: Clinical Features, Treatment, and Nutritional Aspects." Diseases 9, no. 4 (September 23, 2021): 66. http://dx.doi.org/10.3390/diseases9040066.
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Helicobacter pylori (H. pylori) is a 0.5–1 µm wide, 2–4 µm long, short helical, S-shaped Gram-negative microorganism. It is mostly found in the pyloric region of the stomach and causes chronic gastric infection. It is estimated that these bacteria infect more than half of the world’s population. The mode of transmission and infection of H. pylori is still not known exactly, but the faecal–oral and oral–oral routes via water or food consumption are thought to be a very common cause. In the last three decades, research interest has increased regarding the pathogenicity, microbial activity, genetic predisposition, and clinical treatments to understand the severity of gastric atrophy and gastric cancer caused by H. pylori. Studies have suggested a relationship between H. pylori infection and malabsorption of essential micronutrients, and noted that H. pylori infection may affect the prevalence of malnutrition in some risk groups. On the other hand, dietary factors may play a considerably important role in H. pylori infection, and it has been reported that an adequate and balanced diet, especially high fruit and vegetable consumption and low processed salty food consumption, has a protective effect against the outcomes of H. pylori infection. The present review provides an overview of all aspects of H. pylori infection, such as clinical features, treatment, and nutrition.
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Omata, Fumio, Takuro Shimbo, Sachiko Ohde, Gautam A. Deshpande, and Tsuguya Fukui. "Cost-Effectiveness Analysis ofHelicobacter pyloriDiagnostic Methods in Patients with Atrophic Gastritis." Gastroenterology Research and Practice 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/2453254.
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Background. There are several diagnostic methods forHelicobacter pylori (H. pylori)infection. A cost-effective analysis is needed to decide on the optimal diagnostic method. The aim of this study was to determine a cost-effective diagnostic method in patients with atrophic gastritis (AG).Methods. A decision-analysis model including seven diagnostic methods was constructed for patients with AG diagnosed by esophagogastroduodenoscopy. Expected values of cost and effectiveness were calculated for each test.Results. If the prevalence ofH. pyloriin the patients with AG is 85% and CAM-resistantH. pyloriis 30%, histology, stoolH. pyloriantigen (SHPAg), bacterial culture (BC), and urineH. pyloriantibody (UHPAb) were dominated by serumH. pyloriIgG antibody (SHPAb), rapid urease test (RUT), and urea breath test (UBT). Among three undominated methods, the incremental cost-effective ratios (ICER) of RUT versus SHPAb and UBT versus RUT were $214 and $1914, respectively. If the prevalence of CAM-sensitiveH. pyloriwas less than 55%, BC was not dominated, but itsH. pylorieradication success rate was 0.86.Conclusions. RUT was the most cost-effective at the current prevalence of CAM-resistantH. pylori. BC could not be selected due to its poor effectiveness even if CAM-resistantH. pyloriwas more than 45%.
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Schneider, Sabine, Gert Carra, Ugur Sahin, Benjamin Hoy, Gabriele Rieder, and Silja Wessler. "Complex Cellular Responses of Helicobacter pylori-Colonized Gastric Adenocarcinoma Cells." Infection and Immunity 79, no. 6 (March 14, 2011): 2362–71. http://dx.doi.org/10.1128/iai.01350-10.
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ABSTRACTHelicobacter pyloriis an important class I carcinogen that persistently infects the human gastric mucosa to induce gastritis, gastric ulceration, and gastric cancer.H. pyloripathogenesis strongly depends on pathogenic factors, such as VacA (vacuolating cytotoxin A) or a specialized type IV secretion system (T4SS), which injects the oncoprotein CagA (cytotoxin-associated gene A product) into the host cell. Since access to primary gastric epithelial cells is limited, many studies on the complex cellular and molecular mechanisms ofH. pyloriwere performed in immortalized epithelial cells originating from individual human adenocarcinomas. The aim of our study was a comparative analysis of 14 different human gastric epithelial cell lines after colonization withH. pylori. We found remarkable differences in host cell morphology, extent of CagA tyrosine phosphorylation, adhesion to host cells, vacuolization, and interleukin-8 (IL-8) secretion. These data might help in the selection of suitable cell lines to study host cell responses toH. pyloriin vitro, and they imply that different host cell factors are involved in the determination ofH. pyloripathogenesis. A better understanding ofH. pylori-directed cellular responses can provide novel and more balanced insights into the molecular mechanisms ofH. pylori-dependent pathogenesisin vivoand may lead to new therapeutic approaches.
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Blasiak, Janusz, Jan Chojnacki, and Cezary Chojnacki. "Inflammation, oxidative stress, DNA damage response and epigenetic modifications interact behind the beneficial actions of melatonin on H. pylori-mediated gastric disorders." Melatonin Research 6, no. 2 (June 30, 2023): 135–47. http://dx.doi.org/10.32794/mr112500145.
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Helicobacter pylori (H. pylori) infection is associated with several disorders of the gastrointestinal tract, including gastric cancer. Studies of ours and others suggest that H. pylori infection may affect melatonin synthesis in the gastric epithelial cells. On the other hand, melatonin ameliorates gastric disorders as shown in clinical trials and experimental studies. Moreover, melatonin not only suppresses the DNA-damaging reaction of diet-related mutagens that can initiate carcinogenesis in gastric mucosa, but also the oxidative DNA damage evoked by reactive oxygen and nitrogen species produced during H. pylori-related gastric inflammation. H. pylori infection is associated with several functional and organic gastric disorders, including gastritis, peptic ulcer disease and gastric cancer, but the precise mechanism behind this association is not known and many pathways can be involved. Some of beneficial effects of melatonin in the gastrointestinal tract are underlined by mechanisms that likely play a role in detrimental effects of H. pylori in the stomach. Therefore, melatonin may modulate these mechanisms resulting in ameliorating H. pylori-related symptoms. In this narrative review the role of inflammation, oxidative stress, DNA damage response and epigenetic modifications in H. pylori-associated gastric disorders will be discussed with an emphasis on gastric cancer. We also suggest that melatonin may have potential to inhibit H. pylori-mediated pathologies through its interaction with essential pathways as described herein. Overlapping mechanisms of H. pylori-associated pathogenesis and beneficial effects of melatonin justify further studies on the action of melatonin on gastric disorders associated with H. pylori infection, including clinical trials.
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Rao, Prashant, Sarika Mayekar, Vishwajit Pawar, and Mohan Achyut Joshi. "Endoscopic assessment and Helicobacter pylori status evaluation in operated cases of peptic ulcer perforation." International Surgery Journal 7, no. 2 (January 27, 2020): 535. http://dx.doi.org/10.18203/2349-2902.isj20200310.
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Background: Helicobacter pylori’s role in delaying ulcer healing after surgical repair for peptic ulcer perforation causing ulcer persistence hasn’t been definitively established as it has been for uncomplicated ulcers.Methods: Authors performed an endoscopy and H. pylori status evaluation in 30 patients at an average of 6.2 weeks after simple omental patch closure for perforated peptic ulcer.Results: A positive H. pylori status was found in 12 patients (40%) of which 9 had active ulcers. None in the negative group had an active ulcer. H. pylori infection was the only factor found to be responsible for ulcer persistence after surgery.Conclusions: A reasonable approach would thus be to perform an endoscopy 6 weeks after surgery to assess ulcer healing and H. pylori status. H. pylori eradication therapy should then be selectively initialled for patients with an active ulcer or positive H. pylori status.
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Hayashi, Shunji, Toshiro Sugiyama, Ken-Ichi Amano, Hiroshi Isogai, Emiko Isogai, Miki Aihara, Mikio Kikuchi, et al. "Effect of Rebamipide, a Novel Antiulcer Agent, onHelicobacter pylori Adhesion to Gastric Epithelial Cells." Antimicrobial Agents and Chemotherapy 42, no. 8 (August 1, 1998): 1895–99. http://dx.doi.org/10.1128/aac.42.8.1895.
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ABSTRACT Helicobacter pylori is a major etiological agent in gastroduodenal disorders. The adhesion of H. pylori to human gastric epithelial cells is the initial step of H. pylori infection. Inhibition of H. pylori adhesion is thus a therapeutic target in the prevention of H. pyloriinfection. Experiments were performed to evaluate the effect of rebamipide, a novel antiulcer agent, on H. pylori adhesion to gastric epithelial cells. MKN-28 and MKN-45 cells, derived from human gastric carcinomas, were used as target cells. Ten H. pylori strains isolated from patients with chronic gastritis and gastric ulcer were used in the study. We evaluated the effect of rebamipide on H. pylori adhesion to MKN-28 and MKN-45 cells quantitatively using our previously established enzyme-linked immunosorbent assay. The adhesion of H. pylori to MKN-28 and MKN-45 cells was significantly inhibited by pretreatment of these cells with 100 μg of rebamipide per ml. However, the adhesion was not affected by the pretreatment of H. pylori with rebamipide. On the other hand, the viabilities of H. pylori, MKN-28 cells, and MKN-45 cells were not affected by rebamipide. Our studies suggest that rebamipide inhibits the adhesion of H. pylorito gastric epithelial cells.
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Elshenawi, Yasmine, Shuai Hu, and Skander Hathroubi. "Biofilm of Helicobacter pylori: Life Cycle, Features, and Treatment Options." Antibiotics 12, no. 8 (July 31, 2023): 1260. http://dx.doi.org/10.3390/antibiotics12081260.
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Helicobacter pylori is a gastric pathogen that infects nearly half of the global population and is recognized as a group 1 carcinogen by the Word Health Organization. The global rise in antibiotic resistance has increased clinical challenges in treating H. pylori infections. Biofilm growth has been proposed to contribute to H. pylori’s chronic colonization of the host stomach, treatment failures, and the eventual development of gastric diseases. Several components of H. pylori have been identified to promote biofilm growth, and several of these may also facilitate antibiotic tolerance, including the extracellular matrix, outer membrane proteins, shifted morphology, modulated metabolism, efflux pumps, and virulence factors. Recent developments in therapeutic approaches targeting H. pylori biofilm have shown that synthetic compounds, such as small molecule drugs and plant-derived compounds, are effective at eradicating H. pylori biofilms. These combined topics highlight the necessity for biofilm-based research in H. pylori, to improve current H. pylori-targeted therapeutic approaches and alleviate relative public health burden. In this review we discuss recent discoveries that have decoded the life cycle of H. pylori biofilms and current biofilm-targeted treatment strategies.
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Fiorini, Giulia, Ilaria Maria Saracino, Angelo Zullo, Matteo Pavoni, Laura Saccomanno, Tiziana Lazzarotto, Rossana Cavallo, Guido Antonelli, and Berardino Vaira. "Antibiotic Resistance and Therapy for H. pylori Infection in Immigrant Patients Treated in Italy." Journal of Clinical Medicine 9, no. 5 (May 1, 2020): 1299. http://dx.doi.org/10.3390/jcm9051299.
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Background: Helicobacter pylori (H. pylori) infection is the leading cause of both peptic ulcers and gastric tumors, including low-grade MALT-lymphoma and adenocarcinoma. Although it is decreasing in developed countries, H. pylori prevalence remains high in developing areas, mainly due to low socio-economic levels, and the potential consumption of contaminated water. Moreover, a different pattern of primary antibiotic resistance is expected in their H. pylori isolates, potentially affecting the efficacy of standard eradication therapies. Indeed, a previous study showed the eradication rate following triple therapy was distinctly lower in dyspeptic H. pylori infected immigrants living in Italy as compared to Italian patients. Aims: to evaluate the resistance pattern in H. pylori isolates from immigrant patients in Italy, and the success rate of first-line therapy in these patients. Materials and Methods: This retrospective study evaluated data of consecutive immigrant patients, diagnosed with H. pylori infection in a single center (Bologna, Italy) between January 2009 and January 2019. Patients underwent first-line therapy with either sequential or Pylera® (Allergan USA, Inc. Madison, NJ, USA) therapy. Results: A total of 609 immigrants were diagnosed with H. pylori infection during the study period, but 264 previously received an eradication therapy. Therefore, the study was focused on 294 out of 345 naïve patients with a successful bacterial culture with antibiogram. Latin America immigrants had the highest overall resistance rate. Levofloxacin resistance rate was significantly higher in Latin Americans and Asians as compared with Europeans. Based on resistance patterns, sequential therapy showed a clear decreasing trend in eradication rates. Conclusions: while antibiotic resistance rates are generally increasing worldwide, Pylera® seems to achieve a good performance as first-line treatment in all naïve foreigner patients, except for Africans.
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Di Ciaula, Agostino, Giuseppe Scaccianoce, Marino Venerito, Angelo Zullo, Leonilde Bonfrate, Theodore Rokkas, and Piero Portincasa. "Eradication Rates in Italian Subjects Heterogeneously Managed for Helicobacter pylori Infection. Time to Abandon Empiric Treatments in Southern Europe." Journal of Gastrointestinal and Liver Diseases 26, no. 2 (June 1, 2017): 129–37. http://dx.doi.org/10.15403/jgld.2014.1121.262.itl.
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Background & Aims: H. pylori eradication is strongly affected by various factors, including the ongoing antibiotic resistance. We describe a “real life” scenario in patients managed for H. pylori-related conditions, living in a southern Italian region (Apulia), an area with clarithromycin resistance >15%.Methods: 2,224 subjects were studied in two tertiary referral centers in Apulia. Analyses included: reason for referral, H. pylori infection rates (13C-urea breath test – UBT or upper endoscopy), and eradication rates following distinct regimens previously prescribed or prospectively prescribed (such as the bismuth-based quadruple therapy Pylera®, recently marketed in Italy).Results. Over 80% of the patients were referred by family physicians (60% naïve subjects). The overall infection rate was 32.5% and it was similar in asymptomatic patients (31.1%) or with H. pylori-related symptoms/clinical conditions (34.3%). In the 987 H. pylori+ve patients receiving therapy, the overall eradication rate was 80.2% (ITT). Observed eradication rate varied greatly across different regimens: 57.1% (2nd line levofloxacin), 59.6% (unconventional), 70.7% (7-day triple), 73.2% (7-day undefined), 89% (10-day sequential) and 96.9% (ITT, 10 day Pylera®, 1st to 5th line regimens given to 227 patients).Conclusions. A heterogeneous “real life” scenario in Southern Europe shows that H. pylori+ve patients are put at risk of poor outcomes and points to the need of a susceptibility-based therapy according to guidelines and local microbial resistance. In the present setting (i.e. high clarithromycin resistance), despite the high observed eradication rate, sequential therapy should not be recommended (absent in guidelines, unneeded antibiotic). Bismuth-based quadruple treatment (1st, 2nd or subsequent lines) yields the highest eradication rates.Abbreviations: ALT: Altamura; BA: Bari; EGDS: esophagogastroduodenoscopy; GERD: gastro-esophageal reflux disease; H. pylori: Helicobacter pylori; ITT: intention-to-treat; PP: per-protocol; PPI: proton pump inhibitor; UBT: urea breath test.
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I.M., Saracino, Pavoni M., Zullo A., Fiorini G., Saccomanno L., Lazzarotto T., Cavallo R., Antonelli G., and Vaira D. "Antibiotic Resistance and Therapy Outcome in H. pylori Eradication Failure Patients." Antibiotics 9, no. 3 (March 13, 2020): 121. http://dx.doi.org/10.3390/antibiotics9030121.
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Helicobacter pylori (H. pylori) eradication fails in a definite amount of patients despite one or more therapeutic attempts. Curing these patients is progressively more difficult, due to development of antibiotic resistance. Current guidelines suggest testing antibiotic susceptibility in H. pylori isolates following two therapeutic attempts. Aim: to evaluate the development of antibiotic resistance, MIC values trends and therapeutic outcomes in patients who failed at least one H. pylori eradication therapy. Methods: consecutive patients, referred to perform upper gastrointestinal endoscopy (UGIE) to our Unit from January 2009 to January 2019 following at least one therapeutic attempt were considered. Bacterial resistance towards clarithromycin, metronidazole and levofloxacin was tested. Patients received either a susceptibility-guided therapy or Pylera®. Results: a total of 1223 patients were H. pylori positive, and antibiotic susceptibility was available for 1037. The rate of antibiotic resistance and MIC values significantly increased paralleling the number of previous therapeutic attempts. Eradication rates of antibiogram-tailored therapies remained stable, except for the sequential therapy if used as a third line. As a rescue treatment, the Pylera® therapy achieved cure rates comparable to those of the other culture-guided therapies. Conclusions: A significant increase in the secondary resistance towards the three tested antibiotics was observed, both as rate and MIC values, in correlation with the number of therapy failures. These findings should be considered when administering an empirical second-line therapy. Pylera® therapy eradication rates are comparable to culture-tailored therapies.
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Tempera, Patrick Joseph, Mark Michael, Omar Tageldin, and Stephen Hasak. "Gastric Cancer Due to Chronic H. pylori Infection: What We Know and Where We Are Going." Diseases 10, no. 3 (August 25, 2022): 57. http://dx.doi.org/10.3390/diseases10030057.
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Helicobacter pylori is an established cause of many gastrointestinal pathologies including peptic ulcer disease, gastritis, and gastric cancer. It is an entity that affects the global population, and its true nature has only been known since the 1980s. Although there is much known about H. pylori including its pathophysiology, detection, and eradication, resistance to current therapy models is common. This is problematic because untreated or inadequately treated H. pylori increases morbidity and mortality related to gastric cancer and peptic ulcer disease among others. In order to improve the treatment and reduce resistance, there is significant ongoing research identifying new detection and eradication methods for H. pylori. This review aims to highlight what has already been established regarding H. pylori’s epidemiology, pathophysiology, detection, and treatment as well as the most current and novel research involving detection and treatment of H. pylori.
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Sayadishahraki, Masoud, Mahsa Khodadoostan, Hossein Bahrami Samani, Flora Mazaheri, and Somayeh Haghighat. "Body Mass Index and the Success of Helicobacter-pylori Eradication Therapy." Annals of Bariatric Surgery 10, no. 1 (June 30, 2021): 21–26. http://dx.doi.org/10.32598/abs.10.1.1.
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Objective: Helicobacter pylorus (H. pylori) is a gram-negative spiral bacterium related to varieties of gastric and extra-gastric complications. The effects of H. pylori infection on cardiometabolic conditions such as dyslipidemia, diabetes, and metabolic syndrome have to need to be investigated. The present paper aims to assess the effects of body mass index on the success of helicobacter-pylori eradication therapy for the first time. Patients and Methods: This study included 198 patients with H. pylori infection. Patients underwent H. pylori eradication using clarithromycin (500 mg, twice daily, pantoprazole (40 mg, twice daily), amoxicillin (500 mg, three times daily), and bismuth substrate (120 mg, twice daily) for 14 days. After that, the success of eradication was assessed through stool antigen within a month following the treatment. The association of eradication success with age, gender, and BMI were evaluated. Results: H. pylori infection was eradicated in 76.3% (P-value<0.001) of the patients following the eradicative treatment. The rate of response to the anti-H. Pylori remedy was affected by age (P-value=0.29). But it wasn’t affected by gender (P-value=0.81), and BMI (P-value=0.60). Conclusion: Based on the findings of this study, the patientschr('39') response to the H. Pylori eradication was not affected by age, gender, and BMI.
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Samra, Zahoor Qadir, Umber Javaid, Sadia Ghafoor, Aleeza Batool, Nadia Dar, and Muhammad Amin Athar. "PCR assay targeting virulence genes of Helicobacter pylori isolated from drinking water and clinical samples in Lahore metropolitan, Pakistan." Journal of Water and Health 9, no. 1 (February 3, 2011): 208–16. http://dx.doi.org/10.2166/wh.2010.169.
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Helicobacter pylorus is considered for chronic gastritis, gastric ulcers and adenocarcinoma and its high infection rate is observed in overcrowded and lower socioeconomic groups in developing countries. This study was designed to identify the role of drinking water in the transmission and prevalence of H. pylori (HP). Selective HP medium was developed for enrichment and presumptive identification of H. pylori by urease, catalase and species specific 16S rRNA tests. The virulence genes (vacA ‘s’ and ‘m’ regions and cagA) of H. pylori in 90 out of 225 H. pylori positive drinking water samples were present (40%). Ten out of 18 biopsies (55.55%) and 15 out of 50 vomiting fluids of gastric disease patients (30%) were also positive for virulence genes. Anti-H. pylori antibodies were also detected in 31 out of 50 patients’ sera. The presence of virulence genes was also directly confirmed by hybridization studies using non-radioactive DNA probes of 16S rRNA, vacA and cagA genes. The presence of H. pylori in water is due to poor sanitary conditions, improper waste disposal and lack of public health education. PCR-based analysis and colony hybridization can be used for detection of H. pylori in clinical and environmental samples.
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Safatle-Ribeiro, Adriana Vaz, Ulysses Ribeiro Júnior, Angelita Habr-Gama, and Joaquim J. Gama-Rodrigues. "Double pylorus: case report and review of the literature." Revista do Hospital das Clínicas 54, no. 4 (August 1999): 131–34. http://dx.doi.org/10.1590/s0041-87811999000400006.
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Double pylorus is an unusual condition in which a double communication between the gastric antrum and the duodenal bulb occurs. It may be congenital, or it may be acquired complication of peptic ulcer disease. We present a case of double pylorus in a gentleman with epigastric pain and previous history of peptic ulcer disease. The relationship between Helicobacter pylori and this disease was assessed. A review of the literature, the role of associated diseases and the role of H. pylori are discussed.
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German, Serafima V., A. V. Modestova, I. E. Zykova, I. P. Bobrovnitsky, and M. Yu Yakovlev. "ON THE POSSIBLE PARTICULARITY OF HELICOBACTER PYLORI INFECTION TO GALLSTONE DISEASE." Hygiene and sanitation 97, no. 11 (November 15, 2018): 1076–79. http://dx.doi.org/10.18821/0016-9900-2018-97-11-1076-79.
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Introduction. Up to now, it has not been established whether Helicobacter pylori, the most common bacterial pathogen of human, is involved in cholelithiasis. Material and Methods. Based on the analysis of prophylactic medical examination of working people in the Moscow region, the determination the pyloric Helicobacter infection and assessment of the virulence of bacteria there were studied the associations of H. pylori infection and gallstones. The infection was detected by the presence of serum specific antibodies of IgG class, the virulence of the strain H. pylori - by the presence of total antibodies to the protein associated with the cytotoxic gene CagA. There was used enzyme-linked immunosorbent assay. The study included 1,487 people, 931 men and 556 women aged 21-77 years. Results. The H. pylori infection was detected in 1348 (90,6%), CagA protein in - 392 (56.2 %) cases. Gallstones were diagnosed in 72 patients, 21 men (2.3%) and 51 women (9.2%), 67 were seropositive (5% of all infected) and 5 - seronegative (3.6% uninfected). In cholelithiasis cases, the presence of CagA positive strain of H. pylori was investigated in 35 patients. A virulent strain of bacteria was detected in 26 cases (74%), much more often than in the rest examined persons. Conclusion. There were no statistically significant differences in the incidence of cholelithiasis in infected H. pylori and non-infected individuals. A significantly higher prevalence of infection with pathogenic strains of H. pylori in patients with gallstones was found in comparison with the whole group of examined patients, that indicates to the favor of possible involvement of H. pylori infection in this pathology. Confirmation of the role of H. pylori infection as a cumulative risk factor for the gallstones cholecystitis, as well as for other extragastral pathologies, may have an epidemiological, prophylactic, clinical application, due to its widespread prevalence. Further research is needed.
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Negovan, Anca, Andreea-Raluca Szőke, Simona Mocan, and Claudia Bănescu. "Helicobacter pylori-Positive Gastric Biopsies—Association with Clinical Predictors." Life 12, no. 11 (November 4, 2022): 1789. http://dx.doi.org/10.3390/life12111789.
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Introduction: Although Helicobacter pylori’s role in gastric oncogenesis is well-known, only a fraction of infected patients develop cancer. Hence, more factors are supposed to be involved. The objectives of the present study were to investigate the impact of clinicopathological parameters on Helicobacter pylori status. Methods: The study included 1522 patients referred for endoscopy: study group consisted of 557 patients with Helicobacter pylori-positive biopsies confirmed using histochemical stains or immunohistochemistry methods; and the control group consisted of 965 patients with Helicobacter pylori-negative status on histology. Results: Severe endoscopic lesions were more frequent in the Helicobacter pylori group (p < 0.001), with no difference noticed in the distribution of premalignant gastric lesions (p = 0.82). Anemia and dyslipidemia were independent factors associated with Helicobacter pylori-positive biopsies (p < 0.05). Non-steroidal anti-inflammatory therapy was more frequently administered in the study group, while proton-pump inhibitors had an anti-Helicobacter pylori activity on histology (p < 0.0001). Conclusion: In the studied population, patients with Helicobacter pylori-positive biopsies had a more frequent history of gastrotoxic medication, severe endoscopic lesions, and anemia. Helicobacter pylori was unpredictable by gastrointestinal symptoms. The frequency of premalignant gastric lesions was similar irrespective of the actual status of infection, underlining the importance of unintentional clearance of bacteria in old infection and the remaining risk for cancer in this population.
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Watanabe, Tomohiro, Naoki Asano, Atsushi Kitani, Ivan J. Fuss, Tsutomu Chiba, and Warren Strober. "NOD1-Mediated Mucosal Host Defense againstHelicobacter pylori." International Journal of Inflammation 2010 (2010): 1–6. http://dx.doi.org/10.4061/2010/476482.
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Infection of the stomach withHelicobacter pyloriis an important risk factor for gastritis, peptic ulcer, and gastric carcinoma. Although it has been well established that persistent colonization byH. pyloriis associated with adaptive Th1 responses, the innate immune responses leading to these Th1 responses are poorly defined. Recent studies have shown that the activation of nucleotide-binding oligomerization domain 1 (NOD1) in gastric epithelial cells plays an important role in innate immune responses againstH. pylori. The detection ofH. pylori-derived ligands by cytosolic NOD1 induces several host defense factors, including antimicrobial peptides, cytokines, and chemokines. In this paper, we review the molecular mechanisms by which NOD1 contributes to mucosal host defense againstH. pyloriinfection of the stomach.
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Fiorentino, Maria, Hua Ding, Thomas G. Blanchard, Steven J. Czinn, Marcelo B. Sztein, and Alessio Fasano. "Helicobacter pylori-Induced Disruption of Monolayer Permeability and Proinflammatory Cytokine Secretion in Polarized Human Gastric Epithelial Cells." Infection and Immunity 81, no. 3 (January 7, 2013): 876–83. http://dx.doi.org/10.1128/iai.01406-12.
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ABSTRACTHelicobacter pyloriinfection of the stomach is related to the development of diverse gastric pathologies. The ability ofH. pylorito compromise epithelial junctional complexes and to induce proinflammatory cytokines is believed to contribute to pathogenesis. The purpose of this study was to use anin vitrohuman gastric epithelial model to investigate the ability ofH. pylorito affect permeability and the extent and polarity of the host inflammatory response. NCI-N87 monolayers were cocultured with live or heat-killedH. pylorior culture supernatants. Epithelial barrier function was measured by transepithelial electric resistance (TEER) analysis, diffusion of fluorescein isothiocyanate (FITC)-labeled markers, and immunostaining for tight junction proteins. Supernatants from both apical and basolateral chambers were tested for cytokine production by multiplex analysis.H. pyloricaused a significant decrease in TEER, an increased passage of markers through the infected monolayer, and severe disruption and mislocalization of ZO-1 and claudin-1 proteins. Cell viability was not altered byH. pylori, indicating that loss of barrier function could be attributed to a breakdown of tight junction integrity. Significantly high levels of cytokine secretion were induced by either viable or heat-killedH. pylori.H. pyloriaffects monolayer permeability of polarized human gastric epithelial cells. Proinflammatory cytokines were secreted in a polarized manner, mostly basolaterally. Live bacteria are required for disruption of tight junctions but not for the induction of cytokine secretion. The NCI-N87 cell line provides an excellent model for thein vitrostudy ofH. pyloripathogenesis and the epithelial cell host response to infection.
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Bahrami, Ahmad Reza, Ebrahim Rahimi, and Hajieh Ghasemian Safaei. "Detection ofHelicobacter pyloriin City Water, Dental Units' Water, and Bottled Mineral Water in Isfahan, Iran." Scientific World Journal 2013 (2013): 1–5. http://dx.doi.org/10.1155/2013/280510.
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Helicobacter pyloriinfection in human is one of the most common infections worldwide. However, the origin and transmission of this bacterium has not been clearly explained. One of the suggested theories is transmission via water. This study was conducted to determine the prevalence rate ofH. pyloriin tap water, dental units' water, and bottled mineral water in Iran. In the present study, totally 200 water samples were collected in Isfahan province and tested forH. pyloriby cultural method and polymerase chain reaction (PCR) by the detection of theureC (glmM)gene. Using cultural method totally 5 cultures were positive. Two out of 50 tap water samples (4%), 2 out of 35 dental units' water (5.8%) samples, and 1 out of 40 (2.5% ) from water cooler in public places were found to be contaminated withH. pylori.H. pylori ureCgene was detected in 14 (7%) of water samples including 5 tap water (10%), 4 dental units' water (11.4%), 1 refrigerated water with filtration, and 4 (10%) water cooler in public places samples. This may be due to the coccoid form of bacteria which is detected by PCR method.
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Hassan, Md Ali, MA Ahad, MH Rahman, MSH Bhuiyan, and MAH Khan. "Association between cytotoxin producing H. pylori and gastric carcinoma." Bangladesh Medical Journal Khulna 49, no. 1-2 (March 7, 2017): 13–17. http://dx.doi.org/10.3329/bmjk.v49i1-2.31819.
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Background: Enormous studies have been conducted worldwide regarding CagA+ status of H. pylori in gastric carcinoma Objective: No study relating CagA+ status and gastric carcinoma has been carried out in our country yet. This study has been designed to see the association between CagA+ H. pylorl strain and gastric carcinomaMethods: For this purpose, a total number of 80 (eighty) patients were selected. Of the 80 (eighty) patients, 40 (forty) were selected as cases (malignant) and the remainder 40 (forty) were selected as controls (non malignant). H. pylori was detected by applying non invasive (H. pylori IgG serology and CagA-IgG serology) and invasive (Histology and rapid urease test) technique. Of them Histology was done by Modified giemsa stain which was regarded as gold standard, CagA IgG was detected by ELISA method.Results: In this study, among the 40 cases, 35 (thirty five) possess the CagA+ H. pylori strain and among the 40 controls, 33 (thirty three) bear the CagA+ H. pylori strain. In this study, no significant difference between case and control on the point of CagA-IgG status was found.Conclusion: H.pylori may be a simple initiator and not the actual cause of gastric carcinoma.Bang Med J (Khulna) 2016; 49 : 13-17
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Malik, G. M., M. Mubarik, and S. A. Kadla. "Helicobacter pylori Infection in Endoscopic Biopsy Specimens of Gastric Antrum: Laboratory Diagnosis and Comparative Efficacy of Three Diagnostic Tests." Diagnostic and Therapeutic Endoscopy 6, no. 1 (January 1, 1999): 25–29. http://dx.doi.org/10.1155/dte.6.25.
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Aims and objectives The present study was undertaken to compare the diagnostic yield of three available test procedures for detecting Helicobacter pylori (H. pylori) infection in endoscopic biopsies.Methods H. pylori infection was sought in 150 patients referred for upper gastrointestinal (GI) endoscopy. Multiple (about six) biopsy specimens were taken from pyloric antrum in each patient. Two biopsy specimens were subjected to one minute endoscopy room test – OMERT (a modified form of urease test), two were sent for histopathological analysis, where multiple sections were subjected to Giemsa staining and two were sent for microbiological evaluation after Gram's staining of heat fixed biopsy material.Results H. pylori positivity using histology, microbiology and OMERT was observed to be 33%, 30% and 27% respectively. However, overall 40% patients were infected when the results from three test procedures were combined, as H. pylori positivity was repeated more than once by these procedures separately. Histology was found to be superior to other two tests in our study, especially when multiple sections were examined, for the distribution of the organism was patchy. Amongst the infected, H. pylori was seen in only 30% of all 3–8 sections cut from a biopsy, whereas in 70% it was noted in a single section only.Conclusion The study revealed that histology has the highest detection rate and can be chosen as the “gold standard” amongst the three low cost test procedures available at present in our setup.
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Dahshan, Ahmed, Kevin G. Donovan, Issam M. Halabi, Richard Ranne, Mary Li, and William P. Illig. "Helicobacter pylori and Infantile Hypertrophic Pyloric Stenosis." Journal of Pediatric Gastroenterology and Nutrition 42, no. 3 (March 2006): 262–64. http://dx.doi.org/10.1097/01.mpg.0000189359.76545.b8.
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Abadi, Amin Talebi Bezmin, Ashraf Mohabati Mobarez, Omid Teymournejad, and Mona Karbalaei. "Concomitant Colonization ofHelicobacter pyloriin Dental Plaque and Gastric Biopsy." Journal of Pathogens 2014 (2014): 1–4. http://dx.doi.org/10.1155/2014/871601.
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Frequently reportedH. pyloriantimicrobial therapy failures suggest that there might be a different niche where the bacteria can stay safe. Current study aims to examine potential role of oral colonization ofH. pylorito feed reinfection after primary therapy. However, patients who were admitted to the gastroscopy section were chosen and gastric biopsy and dental plaque specimens were collected. Molecular and biochemical tests were applied to confirmH. pyloriidentity in different colonization niches. Results showed that 88.8% of dyspeptic patients had epigastric pains with nocturnal awakening when they were hungry (P=0.023). All patients who received therapy already were again H. pylori positive while they are still carryingH. pyloriin dental plaque (P=0.001). Moreover, H. pylori infection was sought in 100% of gastric biopsy’s dyspeptic patients who had ulcerated esophagitis and erosive duodenitis and who wereH. pyloripositive, and 75% of dyspeptic patients with duodenum deformity had this bacterium in gastric biopsies (P=0.004). Present study showed that only successful eradication of gastricH. pyloricannot guarantee prevention of reinfection. Conclusively, a new strategy which indicates concomitant eradication in oral and gastric colonization can result in clearance ofH. pyloriinfection.
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Lee, Woo-Kon, Keiji Ogura, John T. Loh, Timothy L. Cover, and Douglas E. Berg. "Quantitative Effect of luxS Gene Inactivation on the Fitness of Helicobacter pylori." Applied and Environmental Microbiology 72, no. 10 (August 25, 2006): 6615–22. http://dx.doi.org/10.1128/aem.01291-06.
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ABSTRACT Furanone metabolites called AI-2 (autoinducer 2), used by some bacterial species for signaling and cell density-regulated changes in gene expression, are made while regenerating S-adenosyl methionine (SAM) after its use as a methyl donor. The luxS-encoded enzyme, in particular, participates in this activated methyl cycle by generating both a pentanedione, which is transformed chemically into these AI-2 compounds, and homocysteine, a precursor of methionine and SAM. Helicobacter pylori seems to contain the genes for this activated methyl cycle, including luxS, but not genes for AI-2 uptake and transcriptional regulation. Here we report that deletion of luxS in H. pylori reference strain SS1 diminished its competitive ability in mice and motility in soft agar, whereas no such effect was seen with an equivalent ΔluxS derivative of the unrelated strain X47. These different outcomes are consistent with H. pylori's considerable genetic diversity and are reminiscent of phenotypes seen after deletion of another nonessential metabolic gene, that encoding polyphosphate kinase 1. We suggest that synthesis of AI-2 by H. pylori may be an inadvertent consequence of metabolite flux in its activated methyl cycle and that impairment of this cycle and/or pathways affected by it, rather than loss of quorum sensing, is deleterious for some H. pylori strains. Also tenable is a model in which AI-2 affects other microbes in H. pylori's gastric ecosystem and thereby modulates the gastric environment in ways to which certain H. pylori strains are particularly sensitive.
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Coconnier, Marie-Helene, Vanessa Lievin, Elisabeth Hemery, and Alain L. Servin. "Antagonistic Activity againstHelicobacter Infection In Vitro and In Vivo by the HumanLactobacillus acidophilus Strain LB." Applied and Environmental Microbiology 64, no. 11 (November 1, 1998): 4573–80. http://dx.doi.org/10.1128/aem.64.11.4573-4580.1998.
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ABSTRACT The purpose of the present study was to examine the activity of the human Lactobacillus acidophilus strain LB, which secretes an antibacterial substance(s) against Helicobacter pyloriin vitro and in vivo. The spent culture supernatant (SCS) of the strain LB (LB-SCS) dramatically decreased the viability of H. pylori in vitro independent of pH and lactic acid levels. Adhesion of H. pylori to the cultured human mucosecreting HT29-MTX cells decreased in parallel with the viability of H. pylori. In conventional mice, oral treatment with the LB-SCS protected against infection with Helicobacter felis. Indeed, at both 8 and 49 days post-LB-SCS treatment (29 and 70 days postinfection), inhibition of stomach colonization by H. felis was observed, and no evidence of gastric histopathological lesions was found. LB-SCS treatment inhibits theH. pylori urease activity in vitro and in H. pylori that remained associated with the cultured human mucosecreting HT29-MTX cells. Moreover, a decrease in urease activity was detected in the stomach of the mice infected with H. felis and treated with LB-SCS.
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Tao, Liping, Hai Zou, and Zhimin Huang. "Effects ofHelicobacter pyloriand Heat Shock Protein 70 on the Proliferation of Human Gastric Epithelial Cells." Gastroenterology Research and Practice 2014 (2014): 1–5. http://dx.doi.org/10.1155/2014/794342.
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Infection ofHelicobacter pylori (H. pylori)changed the proliferation of gastric epithelial cells and decreased the expression of heat shock protein 70 (HSP70). However, the effects ofH. pylorion the proliferation of gastric epithelial cells and the roles of HSP70 during the progress need further investigation.Objective.To investigate the effects ofHelicobacter pylori (H. pylori)and heat shock protein 70 (HSP70) on the proliferation of human gastric epithelial cells.Methods. H. pyloriand a human gastric epithelial cell line (AGS) were cocultured. The proliferation of AGS cells was quantitated by an MTT assay, and the expression of HSP70 in AGS cells was detected by Western blotting. HSP70 expression in AGS cells was silenced by small interfering RNA (siRNA) to investigate the role of HSP70. ThesiRNA-treated AGS cells were cocultured withH. pyloriand cell proliferation was measured by an MTT assay.Results.The proliferation of AGS cells was accelerated by coculturing withH. pylorifor 4 and 8 h, but was suppressed at 24 and 48 h. HSP70 expression was decreased in AGS cells infected byH. pylorifor 48 h. The proliferation in HSP70-silenced AGS cells was inhibited after coculturing withH. pylorifor 24 and 48 h compared with the control group.Conclusions.Coculture ofH. pylorialtered the proliferation of gastric epithelial cells and decreased HSP70 expression. HSP70 knockdown supplemented the inhibitory effect ofH. pylorion proliferation of epithelial cells. These results indicate that the effects ofH. pylorion the proliferation of gastric epithelial cells at least partially depend on the decreased expression of HSP70 induced by the bacterium.
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Clyne, Marguerite, and Brendan Drumm. "Adherence ofHelicobacter pylorito the Gastric Mucosa." Canadian Journal of Gastroenterology 11, no. 3 (1997): 243–48. http://dx.doi.org/10.1155/1997/149734.
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Bacterial adhesion to the intestinal epithelium is a critical initial step in the pathogenesis of many enteric diseases.Helicobacter pyloriis a duodenal pathogen that adheres to the gastric epithelium and causes gastritis and peptic ulceration. The mechanism by whichH pyloricauses disease has not yet been elucidated but adherence to the gastric mucosa is thought to be an important virulence determinant of the organism. What is known about adherence ofH pylorito the gastric mucosa is summarized. Topics discussed are the mechanism ofH pyloriadherence; in vitro and in vivo models ofH pyloriinfection; and adherence and potential adhesins and receptors forH pylori.
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Zullo, Angelo, Vincenzo De Francesco, Annamaria Bellesia, Roberto Vassallo, Audenzio D’Angelo, Giuseppe Scaccianoce, Rodolfo Sacco, et al. "Bismuth-based Quadruple Therapy Following H. pylori Eradication Failures: a Multicenter Study in Clinical Practice." Journal of Gastrointestinal and Liver Diseases 26, no. 3 (September 1, 2017): 225–29. http://dx.doi.org/10.15403/jgld.2014.1121.263.zul.
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Background & Aims: Helicobacter pylori (H. pylori) eradication in patients who failed one or more therapeutic attempts remains challenging. This study aimed to assess the efficacy of three-in-one capsules bismuth-based quadruple therapy (Pylera®) in these patients managed in clinical practice.
Methods: This was a prospective, open-label, multicenter study enrolling consecutive, adult patients with persistent H. pylori infection following at least one standard therapy. All patients received a rescue quadruple therapy with Pylera (3 capsules four times daily) and esomeprazole 20 mg (1 tablet twice daily) for 10 days. H. pylori eradication was assessed by using Urea Breath Test 4-6 weeks following therapy ending. H. pylori eradication rates, compliance, and side-effects were calculated.
Results: A total of 208 patients in the 9 participating centres were enrolled. Overall, 180 patients were successfully cured from the infection, accounting for 86.5% (95% CI 81.9-91.2) and 92.3% (95% CI 88.6-96.1) eradication rates at intention-to-treat analysis and at per protocol analysis, respectively. Cure rates were similar across patients who failed one to three previous therapy attempts, but the success rate fell to 67% after 4 or more therapy failures. Compliance to therapy was good in 198 (95.2%) patients, whilst in 7 (5.3%) cases the therapy was interrupted within 5 days due to side effects. A total of 97 (46.6%) patients complained of at least one side effect; nausea, diarrhea and vomiting were the most frequently reported.
Conclusions: Our study found that this bismuth-based quadruple therapy is highly effective as second-line and rescue therapy for H. pylori eradication in clinical practice.
Abbreviations: CI: confidence intervals; ITT: intention-to-treat; PP: per protocol; UBT: urea breath test.
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Chicherin, I. Yu, I. P. Pogorelskiy, E. P. Kolevatykh, I. A. Lundovskikh, and M. R. Shabalina. "First experience with the metaprebiotic Stimbifid plus used for eradication of Helicobacter pylori in patients with gastric ulcer." Infekcionnye bolezni 19, no. 3 (2021): 92–103. http://dx.doi.org/10.20953/1729-9225-2021-3-92-103.
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Objective. To analyze the relationships between probiotic microorganisms and H. pylori KM-11 (RifR) and evaluate their effect on the structural organization of the pathogen and natural colonization resistance of the stomach both independently and with the metaprebiotic Stimbifid plus using bacteriological methods and electron microscopy. Our findings can be potentially used for effective eradication of H. pylori KM-11 (RifR) and treatment of gastric ulcer in volunteers during metaprebiotic therapy. Materials and methods. The following strains of microorganisms were used in this study: Lactobacillus plantarum 8P-A3, Bifidobacterium bifidum No 1, and Helicobacter pylori, isolated from a biopsy specimen of the pyloric antrum collected from a patient with gastritis. A rifampicin-resistant strain of H. pylori KM-11 (RifR) growing on a solid medium with rifampicin (160 μg∙mL–1) was obtained by spontaneous mutagenesis. H. pylori and H. pylori КМ-11 (RifR) were cultivated on hemin containing solid medium with special nutrients at 37°C in an anaerobic cultivation system. Microorganisms were identified by their morphological assessment and using kits for biochemical identification of bacteria. The relationships between probiotic bacteria and H. pylori KM-11 (RifR) were analyzed using the method of paired cultivation on solid and liquid media. The metaprebiotic Stimbifid plus was used in these experiments. Electron microscopy of all microorganisms was performed using a scanning electron microscope. Data analysis was conducted using the Kerber method modified by I.P. Ashmarin and A.A.Vorobyov. Results. Our in vitro experiments with paired cultivation of L. plantarum 8P-A3 and B. bifidum No.1 with H. pylori КМ-11 (RifR) on solid and liquid media containing Stimbifid plus showed that probiotic microorganisms were bioincompatible with H. pylori, i.e. there was an antagonism between a probiotic strain and a pathogenic microorganism. Stimbifid plus added to the cultivation medium acted as an anti-H. pylori agent; moreover, it promoted the restoration of colonization resistance and was a source of exclusive nutrients for probiotic bacteria. Bacteriological testing and electron microscopy demonstrated that the metabolites produced by L. plantarum 8P-A3 can damage the cell wall of H. pylori КМ-11 (RifR) during their co-cultivation in a liquid medium containig Stimbifid plus. This damage appeared as specific changes on the surface of the cell wall and resulted in the loss of viability. Oral administration of Stimbifid plus in six volunteers with gastric ulcer and concomitant severe dysbiosis (with 4 of them tested positive for H. pylori), ensured not only H. pylori eradication and treatment of gastric ulcer, but also confirmed the efficacy of an experimental dose of Stimbifid plus (3000 mg daily for 14 days). Conclusion. The results of our in vitro experiments with cocultivation of probiotic strains L. plantarum 8P-A3 and B. bifidum No 1 with H. pylori КМ-11 (RifR) on solid and liquid media containing Stimbifid plus, as well as experiments with oral administration of Stimbifid plus for H. pylori eradication and treatment of gastric ulcer, demonstrated a substantial therapeutic potential of this metaprebiotic, in particular as a therapy for chronic H. pylori infection and gastric ulcer scarring. Our current results and previous findings on the restoration of colonization resistance, gastric mucosa, and indigenous microbiota, as well as the data on the clearance of pathogenic bacteria in mammals, suggest that Stimbifid plus has a high eradication potential and can be used in clinical practice as a therapeutic agent for acute and chronic infections caused by H. pylori. Key words: Helicobacter pylori, microbiota, colonization resistance, gastric ulcer, eradication, metaprebiotic Stimbifid plus, volunteers
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Kharchenko, Aleksandr V., Nataliya V. Kharchenko, Petro M. Makarenko, Lyudmyla M. Sakharova, Pavlo V. Khomenko, and Olga V. Kvak. "Statistical analysis of the сhronic gastritis in students." Wiadomości Lekarskie 73, no. 2 (2020): 360–64. http://dx.doi.org/10.36740/wlek202002129.
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The aim: The aim of the study is a statistical analysis of the mucosa of the stomach affected by Helicobacter pylori in young people studying at the university. Materials and methods: The work contains the results of the study of chronic gastritis of type B in university volunteer students. The study was attended by students of 1-4 courses, aged 17 to 25 years, a total of 50 people. Among them were 28 men and 22 women. Results: Various forms of chronic gastritis were found in the mucosa of the topographic-anatomical sections of the stomach, 90% of which were associated with Helicobacter pylori (HP). In all departments there is a different amount of common forms of chronic gastritis. In the pyloric section only atrophic gastritis was detected – 31.0 ± 8.5. Atrophic gastritis was also dominant on the lesser curvature – 32.3 ± 7.8, but its forms were significantly (p <0.5) less pronounced than in the pyloric section. In the area of the body, the above variants of chronic gastritis were found in 34.3 ± 8.7 cases, and the majority were flat erosive gastritis 51.0 ± 9.3. There is a tendency to reduce the degree of bacterial contamination of the gastric mucosa from its pyloric section and the lesser curvature to the walls of the body. With a decrease in the degree of bacterial contamination of the gastric mucosa, the degree of leukocyte infiltration also decreases. Between the degree of contamination of the mucous membrane of Helicobacter pylori and the degree of leukocyte infiltration of the mucous membrane, the Pearson correlation coefficient is rxy – 0,935, the correlation is very strong, the coefficient of determination is D=rxy^2 – 0,874, the statistically significant dependence on the probability is 0.99. Conclusions: Atrophic or hyperplastic gastritis associated with HP is found in the gastric mucosa, respectively, 90% of cases. The degree of bacterial contamination correlates with the degree of leukocyte infiltration of the gastric mucosa. Atrophic or hyperplastic gastritis Helicobacter pylori-associated is a common disease of people in young and working age.
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FAISAL, NABIHA, MUHAMMAD MANSOOR UL HAQ, HAFEEZULLAH SHAIKH, Pervez Ashraf, and Jamila H. Esmail. "HELICOBACTER PYLORI INFECTION;." Professional Medical Journal 19, no. 02 (February 22, 2012): 202–7. http://dx.doi.org/10.29309/tpmj/2012.19.02.2011.
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Objective: To determine the frequency of H. pylori infection in dyspeptic patients undergoing endoscopy at a tertiary care centerin Karachi. Data source: Patients undergoing endoscopy at Liaquat National Hospital, Karachi. Design of study: Cross sectional descriptivestudy. Setting: Department of Gastroenterology, Liaquat National Hospital, Karachi. Period: May 2008–October 2008. Material andmethods: All adult patients with symptoms of dyspepsia for more than 1 month duration were included. Patients with upper gastrointestinalbleed, anemia or weight loss were excluded. Upper gastrointestinal endoscopy was performed in all patients and biopsy specimens two eachfrom antrum and body and one from fundus were taken for histology. Results: A total of 123 dyspeptic patients were included in the study. 76(61.8%) patients were males and 47 (38.2%) were females. H pylori was detected in mucosa of 49 (39.8%) patients. The mean age of thepatients was 41.41 ± 13.15 Years (95%CI; 39.06 to 43.75). Rate of H.pylori infection was not found statistical significant with age, gender,duration of symptoms and BMI. Conclusions: The prevalence of H pylori infection in dyspeptic patients was lower than reported in previousstudies from other centers in Pakistan. Other environmental factors should be evaluated in every patient especially who is negative for H. pyloriin our setup.
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Zohaib Hassan, Riaz Ahmed, Sajid Hussain, Muhammad Khalil Surani, Asif Karim, and Mubina Ifat. "Helicobacter pylori infection in children with recurrent abdominal pain." Professional Medical Journal 29, no. 05 (April 30, 2022): 681–85. http://dx.doi.org/10.29309/tpmj/2022.29.05.6822.
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Objective: To find out the frequency of Helicobacter Pylori infection in children with recurrent abdominal pain. Study Design: Cross Sectional study. Setting: Pediatric Medicine, Children Hospital and Institute of Child Health, Multan. Period: November 2020 to May 2021. Material & Methods: A total of 148 children of both genders aged 4-12 years presenting with recurrent abdominal pain were included. Detailed history and physical examination was conducted. Frequency of helicobacter pylori was noted and it association with characteristics of the children studied was noted employing chi square test considering p-value<0.05 as significant. Results: In a total of 148 children with RAP, 83 (56.1%) were male. Overall, mean age was noted to be 7.6±1.9 years while 103 (69.6%) children were aged below 8 years. There were 77 (52%) children who belonged to rural areas whereas 103 (69.6%) were having poor socioeconomic status. Frequency of H. pylori was noted to be positive in 78 (52.7%) children with RAP. Male gender (p=0.001), age between 4-8 years (p=0.012) and poor socioeconomic status (p=0.001) were noted to have significant association with the frequency of H. pylori. Conclusion: Among children with RAP, frequency of H. pylori was very high. The H. pyloi infection was linked with male gender, younger age and low socioeconomic status.
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Kafeel, Asma, Jamshed Bashir, Ishfaq Ahmad Khan, Muhammad Adnan Bawany, Muhammad Javaid Rashid, and Jahana Ara. "Assessment of the Simultaneous Presence of Helicobacter Pylori in the Gastric Mucosa and Gallbladder Mucosa in Patients Suffering from Cholecystitis: a cross Sectional Study." Pakistan Journal of Medical and Health Sciences 16, no. 1 (January 30, 2022): 627–29. http://dx.doi.org/10.53350/pjmhs22161627.
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Aim: The current study was designed to assess the simultaneous presence of H. pylori in gastric and gallbladder mucosa in the patients of acute cholecystitis or symptomatic cholelithiasis. Study design: Cross sectional study Place and duration: This study was conducted at Liaquat University Hospital Hyderabad, Pakistan from March 2020 to March 2021. Methodology: A total of 43 patients suffering from acute cholecystitis and symptomatic cholelithiasis were selected. Their age, gender, and the presence of H. pylori in the gallbladder and gastric mucosa was determined and recorded. The results were statistically analyzed by SPSS version 22. Results: Out of the 43 patients, 20 were male, and 23 were female. Recorded mean age was 54.8±9.9 years and 22 (51.2%) had acute cholecystitis and the remaining 21 (48.8%) had cholelithiasis. In the gastric mucosa, in 14 patients (32.6%) H. pylori was positive. Similarly, in the gall bladder; it was positive in 19 patients (44.2%). In 6 patients (13.9%) i.e. in 4 men and 2 women, H pylori was simultaneously present in both gallbladder and gastric mucosa. No particular relationship was observed in the H. pylori’s presence or absence in gallbladder and gastric mucosa. Conclusion: The presence of H. pylori in gallbladder plays a critical role in the gallbladder’s infection. However, its simultaneous presence in gastric mucosa is not a good standard to assess biliary diseases. Keywords: H. pylori, Cholecystitis, Cholelithiasis, Gallbladder, Gastric mucosa
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Krishnamurthy, Partha, Mary Parlow, Jason B. Zitzer, Nimish B. Vakil, Harry L. T. Mobley, Marilyn Levy, Suhas H. Phadnis, and Bruce E. Dunn. "Helicobacter pylori Containing Only Cytoplasmic Urease Is Susceptible to Acid." Infection and Immunity 66, no. 11 (November 1, 1998): 5060–66. http://dx.doi.org/10.1128/iai.66.11.5060-5066.1998.
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ABSTRACT Helicobacter pylori, an important etiologic agent in a variety of gastroduodenal diseases, produces large amounts of urease as an essential colonization factor. We have demonstrated previously that urease is located within the cytoplasm and on the surface of H. pylori both in vivo and in stationary-phase culture. The purpose of the present study was to assess the relative contributions of cytoplasmic and surface-localized urease to the ability of H. pylori to survive exposure to acid in the presence of urea. Toward this end, we compared the acid resistance in vitro of H. pylori cells which possessed only cytoplasmic urease to that of bacteria which possessed both cytoplasmic and surface-localized or extracellular urease. Bacteria with only cytoplasmic urease activity were generated by using freshly subcultured bacteria or by treating repeatedly subcultured H. pylori with flurofamide (1 μM), a potent, but poorly diffusible urease inhibitor. H. pyloriwith cytoplasmic and surface-located urease activity survived in an acid environment when 5 mM urea was present. In contrast, H. pylori with only cytoplasmic urease shows significantly reduced survival when exposed to acid in the presence of 5 mM urea. Similarly,Escherichia coli SE5000 expressing H. pyloriurease and the Ni2+ transport protein NixA, which expresses cytoplasmic urease activity at levels similar to those in wild-typeH. pylori, survived minimally when exposed to acid in the presence of 5 to 50 mM urea. We conclude that cytoplasmic urease activity alone is not sufficient (although cytoplasmic urease activity is likely to be necessary) to allow survival of H. pyloriin acid; the activity of surface-localized urease is essential for resistance of H. pylori to acid under the assay conditions used. Therefore, the mechanism whereby urease becomes associated with the surface of H. pylori, which involves release of the enzyme from bacteria due to autolysis followed by adsorption of the enzyme to the surface of intact bacteria (“altruistic autolysis”), is essential for survival of H. pylori in an acid environment. The ability of H. pylori to survive exposure to low pH is likely to depend on a combination of both cytoplasmic and surface-associated urease activities.
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Manyakina, O. M., I. S. Akkuratova-Maksimova, T. G. Pukhova, and A. S. Shitova. "Role of genetic structure of Helicobacter Pylori in formation of chronic inflammatory process in gastric mucosa." Perm Medical Journal 38, no. 1 (April 22, 2021): 87–99. http://dx.doi.org/10.17816/pmj38187-99.
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The literature review highlights the questions of the interaction of Helicobacter pylori and the human body. Modern data on the structure of the pathogenicity island in the Helicobacter pylori genome are presented. There is given a detailed description of both well-known virulence and pathogenicity factors of the infection (genes encoding the formation of urease subunits, in particular urel, cytotoxin associated gene A, vacuolating cytotoxin gen A, blood group associated binding adhesion, induced by contact with epithelium) and less studied ones (sialic acid-binding adhesion, adhesion-associated lipoprotein A and B, adhesin gene of Helicobacter pylori, Hp outer membrane protein). The significance of individual genes and proteins encoded by them in the development of chronic inflammatory process in diseases of the upper digestive tract, as well as in ulcer and carcinogenesis is analyzed. Mechanisms of interaction of bacteria with epithelial cells of the gastric mucosa, adhesive and cytotoxic effects of Helicobacter pylori, factors of biofilm formation are described. The influence of the genetic structure of Infect on cytological composition of the gastric glands in the form of reduction of specialized glandular cells chief and parietal cells of pyloric glands and the increase of endocrine cells in the pool is assessed. It is shown that colonization of the gastric mucosa by highly pathogenic strains of Helicobacter pylori contributes to the development of widespread pronounced and active inflammation in it, the appearance of morphological signs of atrophy. The role of the genetic characteristics of the infection in the failure of anti-helicobacter therapy is emphasized. Separately, the question of the effect of combined infection of the gastric mucosa with highly pathogenic strains of Helicobacter pylori and Epstein-Barr virus is highlighted.
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Goto, Takayuki, Akira Nishizono, Toshio Fujioka, Junko Ikewaki, Kumato Mifune, and Masaru Nasu. "Local Secretory Immunoglobulin A and Postimmunization Gastritis Correlate with Protection against Helicobacter pylori Infection after Oral Vaccination of Mice." Infection and Immunity 67, no. 5 (May 1, 1999): 2531–39. http://dx.doi.org/10.1128/iai.67.5.2531-2539.1999.
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ABSTRACT C57BL/6 mice were orally immunized with five weekly doses of 2 mg, 200 μg, or 2 μg of Helicobacter pylori (Sydney strain) whole-cell sonicate combined with cholera toxin. One week after the last vaccination, mice were challenged with 5 × 107CFU of live H. pylori three times at 2-day intervals. At 6 or 18 weeks after the challenge, mice were sacrificed and bacterial cultures and histological studies of the stomach were performed. Vaccination with 2 mg/session or 200 μg/session inhibited H. pylori colonization by 90 and 100%, respectively. These mice were considered protected. Lower levels of H. pylori-specific immunoglobulin A (IgA) were detected in fecal and saliva samples before challenge. However, a significant increase in IgA secretion in mucosal tissue and a higher labeling index for IgA-positive lumina of pyloric glands were noted in these mice in response to challenge and in a vaccine dose-dependent manner. In protected mice, however, severe gastritis characterized by marked infiltration of inflammation mononuclear cells was noted at 6 weeks after challenge, compared with the gastritis seen in unprotected mice or nonvaccinated, ordinarily infected mice. Marked expression of gamma interferon mRNA was detected in the stomach of all protected mice, and 50% of these mice expressed interleukin 4 (IL-4) or IL-5 mRNA. Our findings suggest that local secretory IgA antibody and severe postimmunization gastritis correlate well with protection of mice against H. pylori infection.
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Yamaoka, Yoshio, Kazuyoshi Yamauchi, Hiroyoshi Ota, Atsushi Sugiyama, Satoshi Ishizone, David Y. Graham, Fukuto Maruta, Maki Murakami, and Tsutomu Katsuyama. "Natural History of Gastric Mucosal Cytokine Expression in Helicobacter pylori Gastritis in Mongolian Gerbils." Infection and Immunity 73, no. 4 (April 2005): 2205–12. http://dx.doi.org/10.1128/iai.73.4.2205-2212.2005.
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ABSTRACT Data regarding the chronological changes in gastric mucosal cytokines in the different phases of Helicobacter pylori infection are unavailable. We examined Mongolian gerbils for up to 52 weeks after H. pylori (ATCC 43504) inoculation. Levels of mRNAs of mucosal cytokines (interleukin-1β [IL-1β], gamma interferon [IFN-γ], IL-4, IL-6, and IL-10) were assessed using real-time reverse transcription-PCR. Starting 26 weeks after H. pylori inoculation, two clinicohistologic patterns appeared: gastric ulcers in 32% and hyperplastic polyps in 68% of gerbils. High levels of mucosal IL-1β mRNA were observed early in the infection, reaching maximum at 4 weeks and then rapidly declining. Mucosal IFN-γ mRNA also reached maximal levels at 4 weeks but remained high thereafter. Both IL-1β and IFN-γ mRNA levels were consistently higher in the pyloric mucosa than in the fundic mucosa. In contrast, IL-4, IL-6, and IL-10 mRNA levels peaked at 8 to 26 weeks and levels were similar in the pyloric mucosa and the fundic mucosa. IFN-γ mRNA levels were significantly higher in gerbils with ulcers than in those with hyperplastic polyps (median IFN-γ/glyceraldehyde-3-phosphate dehydrogenase ratio × 100,000 = 650 versus 338, respectively [antrum], and 172 versus 40, respectively [corpus]) (P < 0.05). We propose that the different outcomes (e.g., ulcers or hyperplastic polyps) might relate to imbalances among cytokines.
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de Klerk, Nele, Lisa Maudsdotter, Hanna Gebreegziabher, Sunil D. Saroj, Beatrice Eriksson, Olaspers Sara Eriksson, Stefan Roos, Sara Lindén, Hong Sjölinder, and Ann-Beth Jonsson. "Lactobacilli Reduce Helicobacter pylori Attachment to Host Gastric Epithelial Cells by Inhibiting Adhesion Gene Expression." Infection and Immunity 84, no. 5 (February 29, 2016): 1526–35. http://dx.doi.org/10.1128/iai.00163-16.
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The human gastrointestinal tract, including the harsh environment of the stomach, harbors a large variety of bacteria, of whichLactobacillusspecies are prominent members. The molecular mechanisms by which species of lactobacilli interfere with pathogen colonization are not fully characterized. In this study, we aimed to study the effect of lactobacillus strains upon the initial attachment ofHelicobacter pylorito host cells. Here we report a novel mechanism by which lactobacilli inhibit adherence of the gastric pathogenH. pylori. In a screen withLactobacillusisolates, we found that only a few could reduce adherence ofH. pylorito gastric epithelial cells. Decreased attachment was not due to competition for space or to lactobacillus-mediated killing of the pathogen. Instead, we show that lactobacilli act onH. pyloridirectly by an effector molecule that is released into the medium. This effector molecule acts onH. pyloriby inhibiting expression of the adhesin-encoding genesabA. Finally, we verified that inhibitory lactobacilli reducedH. pyloricolonization in anin vivomodel. In conclusion, certainLactobacillusstrains affect pathogen adherence by inhibitingsabAexpression and thereby reducingH. pyloribinding capacity.
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. "NSAID, gebruikNSAID-gebruik en H. pylori, tetracycline H. pylori, naproxen H. pylori, metronidazol H. pylori, bismutoxideH. Pylori-eradicatie." Medisch-Farmaceutische Mededelingen 38, no. 4 (April 2000): 72. http://dx.doi.org/10.1007/bf03057514.
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NICOLAYSEN, J. "Carcinoma pylori; resectio pylori; död." Nordiskt Medicinskt Arkiv 13, no. 27 (April 24, 2009): 1–12. http://dx.doi.org/10.1111/j.0954-6820.1881.tb00952.x.
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Uthansingh, Kanishka, Ratna Kumari, Girish Kumar Pati, Manas Kumar Behera, Mahesh Chandra Sahu, Jimmy Narayan, Swarup Kumar Patnaik, Pradeep Mallick, and Manoj Kumar Sahu. "Molecular Docking of Anti Helicobacter pylori Antibiotics and Proton Pump Inhibitor: A Single Center Survey." Journal of Pure and Applied Microbiology 15, no. 4 (October 2, 2021): 2103–16. http://dx.doi.org/10.22207/jpam.15.4.33.
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Helicobacter pylorus (H. pylori) is a deadly bacterium responsible for significant worldwide Gastric Cancer (GC) related mortality. The present study aimed to screen all the anti-microbial drugs used to eradicate H .pylori infection and to identify the most efficient drug by using computational methods through molecular docking analysis. The 3-D structure of protein chorismate synthase of H. pylori was downloaded from the Protein data bank (PDB) online browser. The x-ray crystallography structures of 13 common drugs used against H.pylori infection were also downloaded from the drug bank. We screened all 13 common drugs through molecular docking to know the most efficient binding interaction between the diverse ligand-protein complexes. The results were further compared with clinical survey data from the patients with diverse gastrointestinal H. pylori infected cases. Among the screened compounds, by in-silico approach we found that fluoroquinolone (FLRQ) and tetracycline (TET) manifested more significant interactions with chorismate synthase (CS) protein along with binding energies of -9.2 and -8.1 kcal/mole respectively. Further, the drugs were also corroborated with the survey data from patients with varied gastrointestinal disorders in our study. With this computational study, we could find FLRQ and TET may be the most efficient drug for H. pylori treatment, which can be tried in case of anti H. Pylori treatment failure due to resistance. Hence, effective inter-analysis between the experimental and computational approaches is crucial to build up a strong inhibitor.
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Terebiznik, M. R., C. L. Vazquez, K. Torbicki, D. Banks, T. Wang, W. Hong, S. R. Blanke, M. I. Colombo, and N. L. Jones. "Helicobacter pylori VacA Toxin Promotes Bacterial Intracellular Survival in Gastric Epithelial Cells." Infection and Immunity 74, no. 12 (September 25, 2006): 6599–614. http://dx.doi.org/10.1128/iai.01085-06.
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ABSTRACT Helicobacter pylori colonizes the gastric epithelium of at least 50% of the world's human population, playing a causative role in the development of chronic gastritis, peptic ulcers, and gastric adenocarcinoma. Current evidence indicates that H. pylori can invade epithelial cells in the gastric mucosa. However, relatively little is known about the biology of H. pylori invasion and survival in host cells. Here, we analyze both the nature of and the mechanisms responsible for the formation of H. pylori's intracellular niche. We show that in AGS cells infected with H. pylori, bacterium-containing vacuoles originate through the fusion of late endocytic organelles. This process is mediated by the VacA-dependent retention of the small GTPase Rab7. In addition, functional interactions between Rab7 and its downstream effector, Rab-interacting lysosomal protein (RILP), are necessary for the formation of the bacterial compartment since expression of mutant forms of RILP or Rab7 that fail to bind each other impaired the formation of this unique bacterial niche. Moreover, the VacA-mediated sequestration of active Rab7 disrupts the full maturation of vacuoles as assessed by the lack of both colocalization with cathepsin D and degradation of internalized cargo in the H. pylori-containing vacuole. Based on these findings, we propose that the VacA-dependent isolation of the H. pylori-containing vacuole from bactericidal components of the lysosomal pathway promotes bacterial survival and contributes to the persistence of infection.