scholarly journals Chitosan Inhibits Helicobacter pylori Growth and Urease Production and Prevents Its Infection of Human Gastric Carcinoma Cells

Marine Drugs ◽  
2020 ◽  
Vol 18 (11) ◽  
pp. 542
Author(s):  
Shun-Hsien Chang ◽  
Pei-Ling Hsieh ◽  
Guo-Jane Tsai
Keyword(s):  
Helicobacter Pylori ◽  
Culture Medium ◽  
Fluorescent Microscopy ◽  
Inhibitory Effect ◽  
Carcinoma Cells ◽  
Inhibitory Effects ◽  
Urease Production ◽  
Decreasing Ph ◽  
H Pylori ◽  
Human Gastric Carcinoma Cells

This study investigated the effects of shrimp chitosan with 95% degree of deacetylation (DD95) in combination with clinical antibiotics on the growth and urease production of Helicobacter pylori. The inhibitory effect of DD95 on the adherence of H. pylori to the human intestinal carcinoma cells (TSGH9201) was also investigated. Five strains of H. pylori, including three standard strains and two strains of clinical isolates were used as the test strains. The inhibitory effects of DD95 on growth and urease production of various strains of H. pylori increased with increasing DD95 concentration and decreasing pH values from pH 6.0 to pH 2.0. Urease activity of H. pylori at pH 2.0 in the presence of 4000 μg/mL of DD95 decreased by 37.86% to 46.53%. In the presence of 50 μg/mL antibiotics of amoxicillin, tetracycline, or metronidazole at pH 6.0 and pH 2.0, H. pylori counts were decreased by 1.51–3.19, and 1.47–2.82 Log CFU/mL, respectively. Following the addition of 4000 μg/mL DD95 into the 50 μg/mL antibiotic-containing culture medium with pH 6.0 and pH 2.0, overall H. pylori counts were strongly decreased by 3.67–7.61 and 6.61–6.70 Log CFU/mL, respectively. Further, DD95 could inhibit the adherence of H. pylori on TSGH 9201 cells, as evidenced by fluorescent microscopy and thus may potentially protect against H. pylori infection.

scholarly journals Myricetin as an Antivirulence Compound Interfering with a Morphological Transformation into Coccoid Forms and Potentiating Activity of Antibiotics against Helicobacter pylori

2021 ◽  
Vol 22 (5) ◽  
pp. 2695
Author(s):  
Paweł Krzyżek ◽  
Paweł Migdał ◽  
Emil Paluch ◽  
Magdalena Karwańska ◽  
Alina Wieliczko ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Biofilm Formation ◽  
Inhibitory Effect ◽  
Morphological Transformation ◽  
High Tendency ◽  
Minimal Inhibitory Concentrations ◽  
Coccoid Form ◽  
Stomach Diseases ◽  
Fold Reduction ◽  
H Pylori

Helicobacter pylori, a gastric pathogen associated with a broad range of stomach diseases, has a high tendency to become resistant to antibiotics. One of the most important factors related to therapeutic failures is its ability to change from a spiral to a coccoid form. Therefore, the main aim of our original article was to determine the influence of myricetin, a natural compound with an antivirulence action, on the morphological transformation of H. pylori and check the potential of myricetin to increase the activity of antibiotics against this pathogen. We observed that sub-minimal inhibitory concentrations (sub-MICs) of this compound have the ability to slow down the process of transformation into coccoid forms and reduce biofilm formation of this bacterium. Using checkerboard assays, we noticed that the exposure of H. pylori to sub-MICs of myricetin enabled a 4–16-fold reduction in MICs of all classically used antibiotics (amoxicillin, clarithromycin, tetracycline, metronidazole, and levofloxacin). Additionally, RT-qPCR studies of genes related to the H. pylori morphogenesis showed a decrease in their expression during exposure to myricetin. This inhibitory effect was more strongly seen for genes involved in the muropeptide monomers shortening (csd3, csd6, csd4, and amiA), suggesting their significant participation in the spiral-to-coccoid transition. To our knowledge, this is the first research showing the ability of any compound to synergistically interact with all five antibiotics against H. pylori and the first one showing the capacity of a natural substance to interfere with the morphological transition of H. pylori from spiral to coccoid forms.

scholarly journals Effects of vaccination by a recombinant antigen ureB138 (a segment of the β-subunit of urease) against Helicobacter pylori infection

2007 ◽  
Vol 56 (6) ◽  
pp. 847-853 ◽  
Author(s):  
Fumiko Morihara ◽  
Ryoji Fujii ◽  
Emi Hifumi ◽  
Akira Nishizono ◽  
Taizo Uda
Keyword(s):  
Helicobacter Pylori ◽  
Mononuclear Cells ◽  
Gel Filtration ◽  
Immunohistochemical Analysis ◽  
Inhibitory Effect ◽  
Enzymic Activity ◽  
Amino Acid Sequences ◽  
Glutathione S Transferase ◽  
Important Region ◽  
H Pylori

Helicobacter pylori has to counteract acidity during colonization in the stomach. The most important region for the enzymic activity of H. pylori urease, consisting of 138 aa (ureB138), was determined by a comparison of the homology of amino acid sequences, and a structural analysis, between urease of H. pylori and various other species. This region was expressed in Escherichia coli as a fusion protein with glutathione S-transferase (GST), which was cleaved by PreScission protease between the GST moiety and ureB138. The ureB138 protein was then purified by gel filtration. The polyclonal antibody (pAb) induced by immunization with the purified ureB138 could suppress urease activity by about 50 %, while the pAb against the H. pylori urease did not show any inhibitory effect at all. Immunohistochemical analysis indicated that the ureB138-specific pAb specifically recognized the H. pylori infecting human gastric tissues. The effects of vaccination of recombinant ureB138 against infection by this organism were also examined. Specific IgG and IgA antibodies against H. pylori urease were induced in the serum of mice immunized with ureB138. A reduction in the number of colonizing H. pylori was observed in mice treated with ureB138 compared to ones treated with BSA and infection control mice. In the protected mice, severe gastritis characterized by marked infiltration of mononuclear cells was noted compared with the gastritis observed in unprotected mice. Immunohistochemical staining for IgA in gastric mucosa showed that the number of mice positively stained with IgA was significantly higher in ureB138-vaccinated mice than in non-vaccinated mice. This indicates that local IgA antibody and severe post-immunization gastritis correlate well with the protection of mice against H. pylori infection.

Lupeol enhances inhibitory effect of 5-fluorouracil on human gastric carcinoma cells

2016 ◽  
Vol 389 (5) ◽  
pp. 477-484 ◽  
Author(s):  
Yan Liu ◽  
Tingting Bi ◽  
Wei Dai ◽  
Gang Wang ◽  
Liqiang Qian ◽  
...  
Keyword(s):  
Gastric Carcinoma ◽  
Inhibitory Effect ◽  
Carcinoma Cells ◽  
Human Gastric Carcinoma ◽  
Human Gastric Carcinoma Cells

scholarly journals Growth Supplements for Helicobacter pylori

2000 ◽  
Vol 38 (5) ◽  
pp. 1984-1987 ◽  
Author(s):  
Xiuping Jiang ◽  
Michael P. Doyle
Keyword(s):  
Helicobacter Pylori ◽  
Ferrous Sulfate ◽  
Growth Response ◽  
Culture Media ◽  
Horse Serum ◽  
Brain Heart Infusion ◽  
Lag Time ◽  
Inhibitory Effects ◽  
Sodium Pyruvate ◽  
H Pylori

The growth response of Helicobacter pylori in broth was determined in the presence of ferrous sulfate, sodium pyruvate, and mucin (porcine stomach). The addition of either ferrous sulfate and sodium pyruvate or mucin to brain heart infusion broth with 7% horse serum (BHI-HS) enhanced the growth of H. pylori. The best growth of strain NB2-1, which was the slowest growing of 10 H. pylori strains evaluated, occurred in the presence of 0.05% ferrous sulfate and 0.05% sodium pyruvate. The addition of 0.3% mucin to BHI-HS reduced the lag time of H. pylori by 48 h and enhanced the growth. On the basis of the results for 10 H. pylori strains, the combination of ferrous sulfate (0.025%), sodium pyruvate (0.025%), and mucin (0.15%) in BHI-HS counteracted the inhibitory effects of the antibiotics used in culture media for selective growth of H. pylori. Results suggest that these supplements may be useful for enhancement of the growth of H. pylori in enrichment media.

In vitro inhibition ofHelicobacter pyloribyEnterococcus faeciumGM-1

2005 ◽  
Vol 51 (8) ◽  
pp. 629-636 ◽  
Author(s):  
J H Kang ◽  
M S Lee
Keyword(s):  
Helicobacter Pylori ◽  
Inhibitory Activity ◽  
Enterococcus Faecium ◽  
Culture Supernatant ◽  
Proteolytic Enzymes ◽  
Cell Structure ◽  
Inhibitory Effects ◽  
Biochemical Tests ◽  
H Pylori

A strain of Enterococcus faecium that exhibits antibacterial activity against Helicobacter pylori was isolated from the feces of newborn babies. This strain was selected for its ability to inhibit the growth of H. pylori and to withstand harsh environmental conditions, such as acidic pH and high bile concentration. Biochemical tests and 16S rRNA sequencing specific for Enterococcus faecium GM-1 were used to identify the isolated bacterial strain. In vitro studies were used to investigate the inhibitory effects of E. faecium GM-1 on H. pylori. These results showed that the culture supernatant of E. faecium GM-1 significantly decreased the viability and urease activity of H. pylori. This inhibitory activity remained after adjustment of pH of culture supernatant to neutral. However, treatment with proteolytic enzymes reduced the anti-H. pylori activity of GM-1. Therefore, some substance(s) of E. faecium GM-1 other than pH and lactic acid might be associated with this inhibitory activity. Analysis by electron microscopy also demonstrated that the addition of GM-1 destroyed the cell structure of H. pylori. Additional studies suggested that the binding of H. pylori to human colonial cells decreased in the presence of GM-1.Key words: Enterococcus faecium, Helicobacter pylori, inhibition, human fecal strain, proteinaceous substance(s).

The inhibitory effect of lovastatin on the growth of human gastric carcinoma cells in vitro

2001 ◽  
Vol 120 (5) ◽  
pp. A616
Author(s):  
Jayoung Koo ◽  
Wonsup Oh ◽  
Kunyoung Park ◽  
Mooin Park ◽  
Seunja Park
Keyword(s):  
Gastric Carcinoma ◽  
Inhibitory Effect ◽  
Carcinoma Cells ◽  
Human Gastric Carcinoma ◽  
Human Gastric Carcinoma Cells

Analysis of the microbial ecology between Helicobacter pylori and the gastric microbiota of Mongolian gerbils

2014 ◽  
Vol 63 (1) ◽  
pp. 129-137 ◽  
Author(s):  
Cynthia Zaman ◽  
Takako Osaki ◽  
Tomoko Hanawa ◽  
Hideo Yonezawa ◽  
Satoshi Kurata ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Microbial Ecology ◽  
Inhibitory Effect ◽  
Mongolian Gerbils ◽  
Group 2 ◽  
H Pylori ◽  
Gastric Microbiota ◽  
Group 1

Animal models are essential for in vivo analysis of Helicobacter-related diseases. Mongolian gerbils are used frequently to study Helicobacter pylori-induced gastritis and its consequences. The presence of some gastric microbiota with a suppressive effect on H. pylori suggests inhibitory gastric bacteria against H. pylori infection. The aim of the present study was to analyse the microbial ecology between H. pylori and the gastric microbiota of Mongolian gerbils. Gastric mucosa samples of H. pylori-negative and -positive gerbils were orally inoculated to five (Group 1) and six (Group 2) gerbils, respectively, and the gerbils were challenged with H. pylori infection. The colonization rate (40 %) of H. pylori in Group 1 gerbils was lower than the rate (67 %) in Group 2 gerbils. Culture filtrate of the gastric mucosa samples of Group 1 gerbils inhibited the in vitro growth of H. pylori. Three lactobacilli species, Lactobacillus reuteri, Lactobacillus johnsonii and Lactobacillus murinus, were isolated by anaerobic culture from the gerbils in Groups 1 and 2, and identified by genomic sequencing. It was demonstrated that the three different strains of lactobacilli exhibited an inhibitory effect on the in vitro growth of H. pylori. The results suggested that lactobacilli are the dominant gastric microbiota of Mongolian gerbils and the three lactobacilli isolated from the gastric mucosa samples with an inhibitory effect on H. pylori might have an anti-infective effect against H. pylori.

scholarly journals Helicobacter Pylori UreB Upregulates the Expression of PD-L1 through Myh9 /mTOR Pathway and Inhibits the Activation of CD8+ T Cells

2020 ◽  
Author(s):  
Jian Wu ◽  
Honghao Wang ◽  
Xia Guo ◽  
Qinzhen Cai ◽  
Tian Xiang ◽  
...  
Keyword(s):  
T Cells ◽  
Helicobacter Pylori ◽  
Cd8 T Cells ◽  
Mtor Inhibitor ◽  
Mtor Pathway ◽  
Host Cells ◽  
Regulation Mechanism ◽  
Inhibitory Effects ◽  
Culture Model ◽  
H Pylori

Abstract Objectives: Immune regulation mechanism of how Helicobacter pylori urease disrupting the homeostasis of host cells remains unknown.Methods: We thus detected the effect of Helicobacter pylori UreB on macrophage PD-L1 expression with recombinant protein and defective strains. The influence of UreB induced PD-L1 on CD8+ T cells’ proliferation and perforin and granzyme expression were assessed through co-culture model. Results: Urease subset B (UreB) significantly promoted PD-L1 expression in Bone marrow-derived macrophages (BMDMs) and thus blocked the proliferation and activity of H. pylori-primed CD8+ T cells. Myosin heavy chain 9 (Myh9) works as the receptor for UreB. The interaction between UreB and Myh9 promoted amino acid anabolism, activated mTOR pathway and induced PD-L1 expression in BMDMs. mTOR inhibitor Temsirolimus reversed UreB-induced PD-L1 expression and the inhibitory effects on CD8+ T cells. Conclusion: Our study reveals a hitherto-unknown immunosuppressive mechanism of UreB during H. pylori infection, provides clues for the development of H. pylori vaccine.

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