Investigating Helicobacter pylori-related pyloric hypomotility; Functional, histological and molecular alterations

2021 ◽  
Author(s):  
Aya Aly Ashraf ◽  
Sarah Mahmoud Gamal ◽  
Hend Ashour ◽  
Basma Emad Aboulhoda ◽  
Laila Ahmed Rashed ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Smooth Muscle ◽  
Triple Therapy ◽  
Epithelial To Mesenchymal Transition ◽  
Ex Vivo ◽  
Vehicle Group ◽  
Mesenchymal Transition ◽  
H Pylori ◽  
Serum Ghrelin ◽  
E Cadherin

Multiple theories have been proposed describing the pathogenic mechanisms of Helicobacter pylori (H. pylori)-associated gastric motility disorders. We assessed ex-vivo pyloric activity in h.pylori infected rats, and tried to explore the associated ghrelin hormone alteration and pyloric fibrogenesis. In addition, miR-1 was assessed in pyloric tissue samples, being recently accused of having a role in smooth muscle dysfunction. Ninety adult male Wistar albino rats were assigned into 9 groups: 1)Control group, 2)Sterile broth (vehicle group), 3)amoxicillin control, 4) omeperazole control, 5)clarithromycin control, 6)triple therapy control, 7)H. pylori- group, 8)H. pylori-clarithromycin group, and 9)H.pylori-triple therapy group. Urease enzyme activity was applied as an indicator of H. pylori infection. Ex-vivo pyloric contractility was evaluated. Serum ghrelin was assessed, and histological tissue evaluation was performed. Besides, pyloric muscle miR-1 expression was measured. The immunological epithelial to mesenchymal transition (EMT) markers; transforming growth factor β (TGFβ), alpha-smooth muscle actin (α-SMA) and E-cadherin-3 were also evaluated. By H. pylori infection, a significant (P<0.001) reduced pyloric contractility index was recorded. The miR-1 expression was decreased (P<0.001) in the H. pylori-infected group, associated with reduced serum ghrelin, elevated TGFβ, and α-SMA levels and reduced E-cadherin levels. Decreased miR-1 and disturbed molecular pattern were improved by treatment. In conclusion: H. pylori infection was associated with reduced miR-1, epithelial to mesenchymal transition, and pyloric hypomotility. The miR-1 may be a target for further studies to assess its possible involvement in H.pylori associated pyloric dysfunction, which might help in management of human H. pylori manifestations and complications.

scholarly journals Infection with CagA+Helicobacter pylori induces epithelial to mesenchymal transition in human cholangiocytes

2020 ◽  
Author(s):  
Prissadee Thanaphongdecha ◽  
Shannon E. Karinshak ◽  
Wannaporn Ittiprasert ◽  
Victoria H. Mann ◽  
Yaovalux Chamgramol ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial To Mesenchymal Transition ◽  
Cellular Proliferation ◽  
Stem Cell Marker ◽  
Migration And Invasion ◽  
Cell Contact ◽  
Cell Of Origin ◽  
Mesenchymal Transition ◽  
H Pylori

AbstractRecent reports suggest that the East Asian liver fluke, Opisthorchis viverrini, infection with which is implicated in opisthorchiasis-associated cholangiocarcinoma, serves as a reservoir of Helicobacter pylori. The opisthorchiasis-affected cholangiocytes that line the intrahepatic biliary tract are considered to be the cell of origin of this malignancy. Here, we investigated interactions in vitro among human cholangiocytes, a CagA-positive strain of Helicobacter pylori, and the related bacillus, Helicobacter bilis. Exposure to increasing numbers of H. pylori at 0, 1, 10, 100 bacilli per cholangiocyte induced phenotypic changes including the profusion of thread-like filopodia and a loss of cell-cell contact, in a dose-dependent fashion. In parallel, following exposure to H. pylori, changes were evident in levels of mRNA expression of epithelial to mesenchymal transition (EMT)-encoding factors including snail, slug, vimentin, matrix metalloprotease, zinc finger E-box-binding homeobox, and the cancer stem cell marker CD44. Transcription levels encoding the cell adhesion marker CD24 decreased. Analysis to quantify cellular proliferation, migration and invasion in real time using the xCELLigence approach revealed that exposure to ≥10 H. pylori stimulated migration and invasion by the cholangiocytes through an extracellular matrix. In addition, 10 bacilli of CagA-positive H. pylori stimulated contact-independent colony establishment in soft agar. These findings support the hypothesis that infection with H. pylori contributes to the malignant transformation of the biliary epithelium.

scholarly journals Infection with Helicobacter pylori Induces Epithelial to Mesenchymal Transition in Human Cholangiocytes

Pathogens ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 971
Author(s):  
Prissadee Thanaphongdecha ◽  
Shannon E. Karinshak ◽  
Wannaporn Ittiprasert ◽  
Victoria H. Mann ◽  
Yaovalux Chamgramol ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial To Mesenchymal Transition ◽  
Cellular Proliferation ◽  
Stem Cell Marker ◽  
Migration And Invasion ◽  
Cell Contact ◽  
Cell Of Origin ◽  
Mesenchymal Transition ◽  
H Pylori

Recent reports suggest that the East Asian liver fluke infection, caused by Opisthorchis viverrini, which is implicated in opisthorchiasis-associated cholangiocarcinoma, serves as a reservoir of Helicobacter pylori. The opisthorchiasis-affected cholangiocytes that line the intrahepatic biliary tract are considered to be the cell of origin of this malignancy. Here, we investigated interactions in vitro among human cholangiocytes, Helicobacter pylori strain NCTC 11637, and the congeneric bacillus, Helicobacter bilis. Exposure to increasing numbers of H. pylori at 0, 1, 10, 100 bacilli per cholangiocyte of the H69 cell line induced phenotypic changes including the profusion of thread-like filopodia and a loss of cell-cell contact, in a dose-dependent fashion. In parallel, following exposure to H. pylori, changes were evident in levels of mRNA expression of epithelial to mesenchymal transition (EMT)-encoding factors including snail, slug, vimentin, matrix metalloprotease, zinc finger E-box-binding homeobox, and the cancer stem cell marker CD44. Analysis to quantify cellular proliferation, migration, and invasion in real-time by both H69 cholangiocytes and CC-LP-1 line of cholangiocarcinoma cells using the xCELLigence approach and Matrigel matrix revealed that exposure to ≥10 H. pylori bacilli per cell stimulated migration and invasion by the cholangiocytes. In addition, 10 bacilli of H. pylori stimulated contact-independent colony establishment in soft agar. These findings support the hypothesis that infection by H.pylori contributes to the malignant transformation of the biliary epithelium.

Moxifloxacin Based Triple Therapy as Alternative to Standard Therapy in Helicobacter Pylori Eradication.

2020 ◽  
Vol 18 ◽  
Author(s):  
Mohammed Hussien Ahmed ◽  
Sherief Abd-Elsalam ◽  
Aya Mohammed Mahrous
Keyword(s):  
Helicobacter Pylori ◽  
Triple Therapy ◽  
Therapy Group ◽  
Low Cost ◽  
High Rate ◽  
Helicobacter Pylori Eradication ◽  
Treatment Regimens ◽  
Group A ◽  
H Pylori ◽  
Group B

Introduction: Helicobacter pylori eradication remains a problematic issue. We are in an urgent need for finding a treatment regimen that achieves eradication at a low cost and less side effect. Recent published results showing a high rate of resistance and with clarithromycin-based treatment regimens. The aim of the study was to compare moxifloxacin therapy and classic clarithromycin triple therapy in H. pylori eradication. Methods: This was a pilot study that enrolled 60 patients with helicobacter pylori associated gastritis. Diagnosis was done by assessment of H. pylori Ag in the stool. The patients were randomly assigned to receive either moxifloxacin based therapy (Group A), or clarithromycin based therapy (Group B) for two weeks. We stopped the treatment for another two weeks then reevaluation for cure was done. Results: 90 % of patients had negative H. pylori Ag in the stool after 2 weeks of stoppage of the treatment in group A versus 66.7 % in Group B. None of the patients in both groups had major side effects. Conclusion: Moxifloxacin-based therapy showed higher eradication power and less resistance when compared to clarithromycin triple therapy.

Epicardial Cells of Human Adults Can Undergo an Epithelial-to-Mesenchymal Transition and Obtain Characteristics of Smooth Muscle Cells In Vitro

Stem Cells ◽  
2007 ◽  
Vol 25 (2) ◽  
pp. 271-278 ◽  
Author(s):  
John van Tuyn ◽  
Douwe E. Atsma ◽  
Elizabeth M. Winter ◽  
Ietje van der Velde-van Dijke ◽  
Daniel A. Pijnappels ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Muscle Cells ◽  
Mesenchymal Transition ◽  
Epicardial Cells ◽  
Human Adults

Metformin mediated reversal of epithelial to mesenchymal transition is triggered by epigenetic changes in E-cadherin promoter

2016 ◽  
Vol 94 (12) ◽  
pp. 1397-1409 ◽  
Author(s):  
Poulomi Banerjee ◽  
Harshini Surendran ◽  
Debabani Roy Chowdhury ◽  
Karthik Prabhakar ◽  
Rajarshi Pal
Keyword(s):  
Epithelial To Mesenchymal Transition ◽  
Epigenetic Changes ◽  
Mesenchymal Transition ◽  
E Cadherin

scholarly journals Selective killing of Helicobacter pylori with pH-responsive helix–coil conformation transitionable antimicrobial polypeptides

2017 ◽  
Vol 114 (48) ◽  
pp. 12675-12680 ◽  
Author(s):  
Menghua Xiong ◽  
Yan Bao ◽  
Xin Xu ◽  
Hua Wang ◽  
Zhiyuan Han ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Triple Therapy ◽  
Helical Structure ◽  
Commensal Bacteria ◽  
Gastric Ulcers ◽  
Normal Tissues ◽  
Minimal Toxicity ◽  
Antimicrobial Polypeptides ◽  
H Pylori ◽  
Drug Resistant Strains

Current clinical treatment of Helicobacter pylori infection, the main etiological factor in the development of gastritis, gastric ulcers, and gastric carcinoma, requires a combination of at least two antibiotics and one proton pump inhibitor. However, such triple therapy suffers from progressively decreased therapeutic efficacy due to the drug resistance and undesired killing of the commensal bacteria due to poor selectivity. Here, we report the development of antimicrobial polypeptide-based monotherapy, which can specifically kill H. pylori under acidic pH in the stomach while inducing minimal toxicity to commensal bacteria under physiological pH. Specifically, we designed a class of pH-sensitive, helix–coil conformation transitionable antimicrobial polypeptides (HCT-AMPs) (PGA)m-r-(PHLG-MHH)n, bearing randomly distributed negatively charged glutamic acid and positively charged poly(γ-6-N-(methyldihexylammonium)hexyl-l-glutamate) (PHLG-MHH) residues. The HCT-AMPs showed unappreciable toxicity at physiological pH when they adopted random coiled conformation. Under acidic condition in the stomach, they transformed to the helical structure and exhibited potent antibacterial activity against H. pylori, including clinically isolated drug-resistant strains. After oral gavage, the HCT-AMPs afforded comparable H. pylori killing efficacy to the triple-therapy approach while inducing minimal toxicity against normal tissues and commensal bacteria, in comparison with the remarkable killing of commensal bacteria by 65% and 86% in the ileal contents and feces, respectively, following triple therapy. This strategy renders an effective approach to specifically target and kill H. pylori in the stomach while not harming the commensal bacteria/normal tissues.

scholarly journals Helicobacter pylori eradication using tetracycline and furazolidone versus amoxicillin and azithromycin in lansoprazole based triple therapy: an open randomized clinical trial

2005 ◽  
Vol 42 (2) ◽  
pp. 111-115 ◽  
Author(s):  
Laura Cidrão Frota ◽  
Maria do Perpétuo Socorro Saldanha da Cunha ◽  
Carlos René Lima Luz ◽  
Antonio Haroldo de Araujo-Filho ◽  
Luciano A. S. Frota ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Triple Therapy ◽  
Protocol Analysis ◽  
Urea Breath Test ◽  
Test Results ◽  
Suitable Alternative ◽  
Helicobacter Pylori Eradication ◽  
Helicobacter Pylori Treatment ◽  
H Pylori ◽  
To Receive

BACKGROUND: Optimal anti-Helicobacter pylori treatment has not yet been established. AIM: To evaluate H. pylori eradication using tetracycline and furazolidone versus amoxicillin and azithromycin in lansoprazole based triple therapy in northeastern of Brazil. PATIENTS AND METHODS: One hundred and four patients with H. pylori infection, as determined by rapid urease testing and histology, were randomly assigned to receive either: lansoprazole (30 mg q.d.), tetracycline (500 mg q.i.d.), and furazolidone (200 mg t.i.d.) for 7 days (LTF; n = 52); or lansoprazole (30 mg b.i.d.) and amoxicillin (1 g b.i.d.) for 1 week, plus azithromycin (500 mg q.d.) for the first 3 days (LAAz; n = 52). H. pylori eradication was assessed 3 months following completion of therapy by means of rapid urease testing, histology and a 14C-urea breath test. RESULTS: H. pylori eradication was achieved in 46 of 52 (88.4%, 95% CI: 77.5%-95.1%) patients in LTF group and in 14 of 52 (26.9%, 95% CI: 16.2%-40,1%) patients in LAAz group. On a per-protocol analysis, eradication rates were 91.8% (95% CI: 81.4%-97.3%) and 28.5% (95% CI: 17.2%-42.3%), respectively in LTF and LAAz groups. CONCLUSION: The LAAz regimen yielded unacceptably low eradication rates. On the other hand, the LTF scheme represents a suitable alternative for H. pylori eradication.

scholarly journals Afadin Downregulation by Helicobacter pylori Induces Epithelial to Mesenchymal Transition in Gastric Cells

2018 ◽  
Vol 9 ◽  
Author(s):  
Miguel Sardinha Marques ◽  
Joana Melo ◽  
Bruno Cavadas ◽  
Nuno Mendes ◽  
Luísa Pereira ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial To Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Gastric Cells

Epithelial-to-mesenchymal transition in cyst lining epithelial cells in an orthologous PCK rat model of autosomal-recessive polycystic kidney disease

2011 ◽  
Vol 300 (2) ◽  
pp. F511-F520 ◽  
Author(s):  
Hiroko Togawa ◽  
Koichi Nakanishi ◽  
Hironobu Mukaiyama ◽  
Taketsugu Hama ◽  
Yuko Shima ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Epithelial Cells ◽  
Polycystic Kidney Disease ◽  
Autosomal Recessive ◽  
Epithelial To Mesenchymal Transition ◽  
Cell Contact ◽  
Polycystic Kidney ◽  
Mesenchymal Transition ◽  
Cyst Lining ◽  
E Cadherin

In polycystic kidney disease (PKD), cyst lining cells show polarity abnormalities. Recent studies have demonstrated loss of cell contact in cyst cells, suggesting induction of epithelial-to-mesenchymal transition (EMT). Recently, EMT has been implicated in the pathogenesis of PKD. To explore further evidence of EMT in PKD, we examined age- and segment-specific expression of adhesion molecules and mesenchymal markers in PCK rats, an orthologous model of human autosomal-recessive PKD. Kidneys from 5 male PCK and 5 control rats each at 0 days, 1, 3, 10, and 14 wk, and 4 mo of age were serially sectioned and stained with segment-specific markers and antibodies against E-cadherin, Snail1, β-catenin, and N-cadherin. mRNAs for E-cadherin and Snail1 were quantified by real-time PCR. Vimentin, fibronectin, and α-smooth muscle actin (α-SMA) expressions were assessed as mesenchymal markers. E-cadherin expression pattern was correlated with the disease pathology in that tubule segments showing the highest expression in control had much severer cyst formation in PCK rats. In PCK rats, E-cadherin and β-catenin in cystic tubules was attenuated and localized to lateral areas of cell-cell contact, whereas nuclear expression of Snail1 increased in parallel with cyst enlargement. Some epithelial cells in large cysts derived from these segments, especially in adjacent fibrotic areas, showed positive immunoreactivity for vimentin and fibronectin. In conclusion, these findings suggest that epithelial cells in cysts acquire mesenchymal features in response to cyst enlargement and participate in progressive renal fibrosis. Our study clarified the nephron segment-specific cyst profile related to EMT in PCK rats. EMT may play a key role in polycystic kidney disease.

Sign in / Sign up

Export Citation Format

Share Document