scholarly journals In Vitro and In Vivo Inhibition of Helicobacter pylori by Lactobacillus casei Strain Shirota

2004 ◽  
Vol 70 (1) ◽  
pp. 518-526 ◽  
Author(s):  
D. Sgouras ◽  
P. Maragkoudakis ◽  
K. Petraki ◽  
B. Martinez-Gonzalez ◽  
E. Eriotou ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Lactobacillus Casei ◽  
Clinical Isolates ◽  
Mucosal Inflammation ◽  
Control Group ◽  
Study Group ◽  
Milk Product ◽  
H Pylori

ABSTRACT We studied the potential inhibitory effect of Lactobacillus casei strain Shirota (from the fermented milk product Yakult [Yakult Ltd., Tokyo, Japan]) on Helicobacter pylori by using (i) in vitro inhibition assays with H. pylori SS1 (Sydney strain 1) and nine H. pylori clinical isolates and (ii) the in vivo H. pylori SS1 mouse model of infection over a period of 9 months. In vitro activity against H. pylori SS1 and all of the clinical isolates was observed in the presence of viable L. casei strain Shirota cells but not in the cell-free culture supernatant, although there was profound inhibition of urease activity. In vivo experiments were performed by oral administration of L. casei strain Shirota in the water supply over a period of 9 months to 6-week-old C57BL/6 mice previously infected with H. pylori SS1 (study group; n = 25). Appropriate control groups of H. pylori-infected but untreated animals (n = 25) and uninfected animals given L. casei strain Shirota (n = 25) also were included in the study. H. pylori colonization and development of gastritis were assessed at 1, 2, 3, 6, and 9 months postinfection. A significant reduction in the levels of H. pylori colonization was observed in the antrum and body mucosa in vivo in the lactobacillus-treated study group, as assessed by viable cultures, compared to the levels in the H. pylori-infected control group. This reduction was accompanied by a significant decline in the associated chronic and active gastric mucosal inflammation observed at each time point throughout the observation period. A trend toward a decrease in the anti-H. pylori immunoglobulin G response was measured in the serum of the animals treated with lactobacillus, although this decrease was not significant.

scholarly journals 3-Pentylcatechol, a Non-Allergenic Urushiol Derivative, Displays Anti-Helicobacter pylori Activity In Vivo

2020 ◽  
Vol 13 (11) ◽  
pp. 384
Author(s):  
Hang Yeon Jeong ◽  
Tae Ho Lee ◽  
Ju Gyeong Kim ◽  
Sueun Lee ◽  
Changjong Moon ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Triple Therapy ◽  
Inflammatory Cells ◽  
Control Group ◽  
Vitro Assay ◽  
Low Concentrations ◽  
H Pylori ◽  
Stomach Mucous Membrane

We previously reported that 3-pentylcatechol (PC), a synthetic non-allergenic urushiol derivative, inhibited the growth of Helicobacter pylori in an in vitro assay using nutrient agar and broth. In this study, we aimed to investigate the in vivo antimicrobial activity of PC against H. pylori growing in the stomach mucous membrane. Four-week-old male C57BL/6 mice (n = 4) were orally inoculated with H. pylori Sydney Strain-1 (SS-1) for 8 weeks. Thereafter, the mice received PC (1, 5, and 15 mg/kg) and triple therapy (omeprazole, 0.7 mg/kg; metronidazole, 16.7 mg/kg; clarithromycin, 16.7 mg/kg, reference groups) once daily for 10 days. Infiltration of inflammatory cells in gastric tissue was greater in the H. pylori-infected group compared with the control group and lower in both the triple therapy- and PC-treated groups. In addition, upregulation of cytokine mRNA was reversed after infection, upon administration of triple therapy and PC. Interestingly, PC was more effective than triple therapy at all doses, even at 1/15th the dose of triple therapy. In addition, PC demonstrated synergism with triple therapy, even at low concentrations. The results suggest that PC may be more effective against H. pylori than established antibiotics.

scholarly journals In Vitro and In Vivo Antibacterial Activities of Patchouli Alcohol, a Naturally Occurring Tricyclic Sesquiterpene, against Helicobacter pylori Infection

2017 ◽  
Vol 61 (6) ◽  
Author(s):  
Y. F. Xu ◽  
D. W. Lian ◽  
Y. Q. Chen ◽  
Y. F. Cai ◽  
Y. F. Zheng ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Bacterial Resistance ◽  
Clinical Isolates ◽  
Potential Candidate ◽  
Necrosis Factor Alpha ◽  
Content Type ◽  
Patchouli Alcohol ◽  
H Pylori

ABSTRACT This study further evaluated the in vitro and in vivo anti-Helicobacter pylori activities and potential underlying mechanism of patchouli alcohol (PA), a tricyclic sesquiterpene. In the in vitro assay, the capacities of PA to inhibit and kill H. pylori were tested on three standard strains at different pH values and on 12 clinical isolates. The effects of PA on H. pylori adhesion (and its alpA, alpB, and babA genes), motility (and its flaA and flaB genes), ultrastructure, and flagellation were investigated. Moreover, the H. pylori resistance to and postantibiotic effect (PAE) of PA were determined. Furthermore, the in vivo effects of PA on H. pylori eradication and gastritis were examined. Results showed that MICs of PA against three standard strains (pH 5.3 to 9) and 12 clinical isolates were 25 to 75 and 12.5 to 50 μg/ml, respectively. The killing kinetics of PA were time and concentration dependent, and its minimal bactericidal concentrations (MBCs) were 25 to 75 μg/ml. In addition, H. pylori adhesion, motility, ultrastructure, and flagellation were significantly suppressed. PA also remarkably inhibited the expression of adhesion genes (alpA and alpB) and motility genes (flaA and flaB). Furthermore, PA treatment caused a longer PAE and less bacterial resistance than clarithromycin and metronidazole. The in vivo study showed that PA can effectively eradicate H. pylori, inhibit gastritis, and suppress the expression of inflammatory mediators (COX-2, interleukin 1β, tumor necrosis factor alpha, and inducible nitric oxide synthase [iNOS]). In conclusion, PA can efficiently kill H. pylori, interfere with its infection process, and attenuate gastritis with less bacterial resistance, making it a potential candidate for new drug development.

scholarly journals Variations in Helicobacter pylori Lipopolysaccharide To Evade the Innate Immune Component Surfactant Protein D

2005 ◽  
Vol 73 (11) ◽  
pp. 7677-7686 ◽  
Author(s):  
Wafa Khamri ◽  
Anthony P. Moran ◽  
Mulugeta L. Worku ◽  
Q. Najma Karim ◽  
Marjorie M. Walker ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Phase Variation ◽  
Surfactant Protein ◽  
Clinical Isolates ◽  
Surfactant Protein D ◽  
Human Gastric Mucosa ◽  
H Pylori

ABSTRACT Helicobacter pylori is a common and persistent human pathogen of the gastric mucosa. Surfactant protein D (SP-D), a component of innate immunity, is expressed in the human gastric mucosa and is capable of aggregating H. pylori. Wide variation in the SP-D binding affinity to H. pylori has been observed in clinical isolates and laboratory-adapted strains. The aim of this study was to reveal potential mechanisms responsible for evading SP-D binding and establishing persistent infection. An escape variant, J178V, was generated in vitro, and the lipopolysaccharide (LPS) structure of the variant was compared to that of the parental strain, J178. The genetic basis for structural variation was explored by sequencing LPS biosynthesis genes. SP-D binding to clinical isolates was demonstrated by fluorescence-activated cell sorter analyses. Here, we show that H. pylori evades SP-D binding through phase variation in lipopolysaccharide. This phenomenon is linked to changes in the fucosylation of the O chain, which was concomitant with slipped-strand mispairing in a poly(C) tract of the fucosyltransferase A (fucT1) gene. SP-D binding organisms are predominant in mucus in vivo (P = 0.02), suggesting that SP-D facilitates physical elimination. Phase variation to evade SP-D contributes to the persistence of this common gastric pathogen.

scholarly journals Quantitative Detection of Helicobacter pylori Gene Expression In Vivo and Relationship to Gastric Pathology

2000 ◽  
Vol 68 (10) ◽  
pp. 5488-5495 ◽  
Author(s):  
Richard M. Peek ◽  
Leen-Jan van Doorn ◽  
John P. Donahue ◽  
Kyi T. Tham ◽  
Ceu Figueiredo ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
16S Rrna ◽  
Gene Families ◽  
Mucosal Inflammation ◽  
Quantitative Detection ◽  
Biopsy Specimens ◽  
Gene Structures ◽  
H Pylori

ABSTRACT The iceA locus of Helicobacter pyloriincludes one of two mutually exclusive gene families, iceA1and iceA2. Colonization with iceA1 strains is associated with enhanced acute mucosal inflammation, and adherence to gastric epithelial cells in vitro induces expression oficeA1 but not iceA2 mRNA; however, both transcripts can be detected in vivo. The aim of this study was to determine whether differing levels of iceA transcription in vivo may contribute to disease pathogenesis. RNA from 41 H. pylori-positive gastric biopsy specimens was reverse transcribed to cDNA. Quantitative PCR was performed using biotinylated iceA1, iceA2, and 16S rRNA primers, and binding of biotinylated products to streptavidin-coated plates was detected by hybridization with a fluorescein-labeled probe. iceAgenotypes were determined by PCR and sequence analysis. All 41 samples contained detectable H. pylori 16S rRNA, with similar levels in iceA1- (n = 10) andiceA2 (n = 31)-colonized patients (P = 0.34). Biopsy specimens from four (40%) and 19 (61%) persons colonized with iceA1 or iceA2strains, respectively, had detectable iceA RNA. Acute inflammatory scores were significantly higher in iceA1RNA-positive patients than in iceA1 RNA-negative,iceA2 RNA-positive, or iceA2 RNA-negative subjects (P ≤ 0.05 for each). Within theiceA2 RNA-positive group, H. pylori strains with a single 35-amino-acid cassette were associated with significantly higher mucosal iceA2 transcript levels (P= 0.014 versus strains with two cassettes). These results indicate that the levels of transcription of H. pylori iceA1 andiceA2 and of 16S rRNA are independent and that particulariceA2 gene structures are associated with enhanced transcription. The finding that iceA1 transcription levels are significantly associated with the intensity of neutrophilic infiltration suggests that heterogeneity in inflammatory scores among persons colonized with H. pylori iceA1 strains reflects levels of iceA1 transcription in vivo.

scholarly journals Is The Theoretical Knowledge Reflected in Current Practice: Histopathological Helicobacter Pylori Research?

2021 ◽  
Vol 6 (1) ◽  
pp. 22-25
Author(s):  
Mehmet Ali Kosekli ◽  
Keyword(s):  
Helicobacter Pylori ◽  
Public Health Problem ◽  
Clinical Trial Data ◽  
In Vitro Study ◽  
Control Group ◽  
Study Group ◽  
Optimal Test ◽  
Study Results ◽  
H Pylori

Abstract: Objective: Helicobacter pylori (H. pylori) is considered in the category of biological agent directly responsible for cancer. Guidelines recommend discontinuing suppressive conditions prior to histopathological helicobacter pylori testing, but there is little clinical trial data on how outcome is affected if this is not done. Optimal test recommendations in the guidelines are based on in vitro study results. In present study, we aimed to observe whether there was a difference in the prevalence of H. pylori histopathologically in patients who met the necessary prerequisites before Esophago-Gastro-Duodenoscopy (EGD) compared to the subjects group who did not meet the PPI discontinuation condition. Materials & Methods: This retrospective study was conducted between October 2015 and August 2016 in a reference hospital with 1.5 million hinterlands. Patients who underwent EGD by meeting all the prerequisites recommended by the guidelines for the H. pylori test were included in the study group (n=213), and those who discontinued other suppressive drugs except PPI were included in the control group (n=193). Results: While H. pylori was found to be 74.6% positive in the study group that provided all the prerequisites for histopathological H. pylori detection, H. pylori was found to be 64.9% positive in the control group continuing to receive PPI treatment (p=0.02). Conclusion: In conclusion, we suggest that it is necessary to proceed with the guidance of classical knowledge in determining the presence of H. pylori, which is a common public health problem that is up-to-date. Keywords: Helicobacter pylori, Suppressive condition, Proton pump inhibitor, Histopathology, Cancer, Guideline.

Enhanced fitness of a Helicobacter pylori babA mutant in a murine model

2021 ◽  
Author(s):  
M. Lorena Harvey ◽  
Aung Soe Lin ◽  
Lili Sun ◽  
Tatsuki Koyama ◽  
Jennifer H. B. Shuman ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Outer Membrane Proteins ◽  
Population Diversity ◽  
Fitness Advantage ◽  
Neutral Locus ◽  
Mutant Strains ◽  
Bacterial Fitness ◽  
H Pylori

Helicobacter pylori genomes encode >60 predicted outer membrane proteins (OMPs). Several OMPs in the Hop family act as adhesins, but the functions of most Hop proteins are unknown. To identify hop mutant strains that exhibit altered fitness in vivo compared to fitness in vitro , we used a genetic barcoding method that allowed us to track changes in the proportional abundance of H. pylori strains within a mixed population. We generated a library of hop mutant strains, each containing a unique nucleotide barcode, as well as a library of control strains, each containing a nucleotide barcode in an intergenic region predicted to be a neutral locus unrelated to bacterial fitness. We orogastrically inoculated each of the libraries into mice and analyzed compositional changes in the populations over time in vivo compared to changes detected in the populations during library passage in vitro . The control library proliferated as a relatively stable community in vitro, but there was a reduction in the population diversity of this library in vivo and marked variation in the dominant strains recovered from individual animals, consistent with the existence of a non-selective bottleneck in vivo . We did not identify any OMP mutants exhibiting fitness defects exclusively in vivo without corresponding fitness defects in vitro . Conversely, a babA mutant exhibited a strong fitness advantage in vivo but not in vitro . These findings, when taken together with results of other studies, suggest that production of BabA may have differential effects on H. pylori fitness depending on the environmental conditions.

scholarly journals Lactobacillus johnsonii La1 Attenuates Helicobacter pylori-Associated Gastritis and Reduces Levels of Proinflammatory Chemokines in C57BL/6 Mice

2005 ◽  
Vol 12 (12) ◽  
pp. 1378-1386 ◽  
Author(s):  
Dionyssios N. Sgouras ◽  
Effrosini G. Panayotopoulou ◽  
Beatriz Martinez-Gonzalez ◽  
Kalliopi Petraki ◽  
Spyros Michopoulos ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Lamina Propria ◽  
Serum Levels ◽  
Favorable Effect ◽  
Lactobacillus Johnsonii ◽  
Ags Cells ◽  
Inflammatory Infiltration ◽  
H Pylori

ABSTRACT In clinical settings, Lactobacillus johnsonii La1 administration has been reported to have a favorable effect on Helicobacter pylori-associated gastritis, although the mechanism remains unclear. We administered, continuously through the water supply, live La1 to H. pylori-infected C57BL/6 mice and followed colonization, the development of H. pylori-associated gastritis in the lamina propria, and the levels of proinflammatory chemokines macrophage inflammatory protein 2 (MIP-2) and keratinocyte-derived cytokine (KC) in the serum and gastric tissue over a period of 3 months. We documented a significant attenuation in both lymphocytic (P = 0.038) and neutrophilic (P = 0.003) inflammatory infiltration in the lamina propria as well as in the circulating levels of anti-H. pylori immunoglobulin G antibodies (P = 0.003), although we did not observe a suppressive effect of La1 on H. pylori colonizing numbers. Other lactobacilli, such as L. amylovorus DCE 471 and L. acidophilus IBB 801, did not attenuate H. pylori-associated gastritis to the same extent. MIP-2 serum levels were distinctly reduced during the early stages of H. pylori infection in the La1-treated animals, as were gastric mucosal levels of MIP-2 and KC. Finally, we also observed a significant reduction (P = 0.046) in H. pylori-induced interleukin-8 secretion by human adenocarcinoma AGS cells in vitro in the presence of neutralized (pH 6.8) La1 spent culture supernatants, without concomitant loss of H. pylori viability. These observations suggest that during the early infection stages, administration of La1 can attenuate H. pylori-induced gastritis in vivo, possibly by reducing proinflammatory chemotactic signals responsible for the recruitment of lymphocytes and neutrophils in the lamina propria.

scholarly journals Therapeutic effects of Zuojin Pill on Helicobacter pylori-induced chronic atrophic gastritis through JMJD2B/COX-2/VEGF signaling axis

2020 ◽  
Author(s):  
Shihua Wu ◽  
Chunmei Bao ◽  
Ruilin Wang ◽  
Xiaomei Zhang ◽  
Sijia Gao ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Cell Viability ◽  
Atrophic Gastritis ◽  
Chronic Atrophic Gastritis ◽  
Gastric Mucosal Damage ◽  
Therapeutic Effects ◽  
Cox 2 ◽  
H Pylori

Abstract Background: Zuojin Pill (ZJP), a famous Chinese medicinal formula, widely accepted for treatment of chronic atrophic gastritis (CAG) in China. This study aimed to explore the therapeutic effects and mechanisms of ZJP in Helicobacter pylori (H. pylori) - induced chronic atrophic gastritis (CAG) in vivo and in vitro. Methods: CAG rat model was induced by H. pylori. ZJP (0.63, 1.26, and 2.52 g/kg, respectively) was administered orally for four weeks. Therapeutic effects of ZJP were identified by H&E staining and serum indices. In addition, cell viability, morphology and proliferation were detected by cell counting kit-8 (CCK8) and high-content screening assay (HCS), respectively. Moreover, relative mRNA expression and protein expression related to JMJD2B/COX-2/VEGF axis was detected to investigate the potential mechanisms of ZJP in CAG. Results: Results showed the symptoms (weight loss and gastric mucosa damage) of CAG were alleviated, and the contents of TNF-α in serum was markedly decreased after treating with ZJP. Moreover, cell viability, proliferation and morphology changes of GES-1 cells were ameliorated by ZJP intervention. In addition, proinflammatory genes and JMJD2B/COX-2/VEGF axis related genes were suppressed by ZJP administration in vitro and in vivo. Meanwhile, immunohistochemistry (IHC) and western blot confirmed down-regulation of these genes by ZJP intervention. Conclusion: ZJP treatment can alleviate gastric mucosal damage induced by H. pylori via JMJD2B/COX-2/VEGF axis.

scholarly journals A Novel 3-Deoxy-d-manno-Octulosonic Acid (Kdo) Hydrolase That Removes the Outer Kdo Sugar of Helicobacter pylori Lipopolysaccharide

2005 ◽  
Vol 187 (10) ◽  
pp. 3374-3383 ◽  
Author(s):  
Christopher Stead ◽  
An Tran ◽  
Donald Ferguson ◽  
Sara McGrath ◽  
Robert Cotter ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Lipid A ◽  
In Vitro Assay ◽  
Spectrometric Analysis ◽  
Vitro Assay ◽  
The Core ◽  
H Pylori

ABSTRACT The lipid A domain anchors lipopolysaccharide (LPS) to the outer membrane and is typically a disaccharide of glucosamine that is both acylated and phosphorylated. The core and O-antigen carbohydrate domains are linked to the lipid A moiety through the eight-carbon sugar 3-deoxy-d-manno-octulosonic acid known as Kdo. Helicobacter pylori LPS has been characterized as having a single Kdo residue attached to lipid A, predicting in vivo a monofunctional Kdo transferase (WaaA). However, using an in vitro assay system we demonstrate that H. pylori WaaA is a bifunctional enzyme transferring two Kdo sugars to the tetra-acylated lipid A precursor lipid IVA. In the present work we report the discovery of a Kdo hydrolase in membranes of H. pylori capable of removing the outer Kdo sugar from Kdo2-lipid A. Enzymatic removal of the Kdo group was dependent upon prior removal of the 1-phosphate group from the lipid A domain, and mass spectrometric analysis of the reaction product confirmed the enzymatic removal of a single Kdo residue by the Kdo-trimming enzyme. This is the first characterization of a Kdo hydrolase involved in the modification of gram-negative bacterial LPS.

scholarly journals Detection of High Titers of Antibody against Helicobacter Cysteine-Rich Proteins A, B, C, and E in Helicobacter pylori-Infected Individuals

2003 ◽  
Vol 10 (4) ◽  
pp. 542-545 ◽  
Author(s):  
Peer R. E. Mittl ◽  
Lucas Lüthy ◽  
Christoph Reinhardt ◽  
Hellen Joller
Keyword(s):  
Helicobacter Pylori ◽  
Immune System ◽  
Control Group ◽  
Clear Correlation ◽  
Weak Correlation ◽  
The Family ◽  
Genome Level ◽  
Immunological Assays ◽  
H Pylori

ABSTRACT The family of Helicobacter cysteine-rich proteins (Hcp) constitutes one of the largest protein families that are specific for proteobacteria from the delta/epsilon subgroup. Most of the proteins belonging to this family have so far only been recognized on the genome level. To investigate the expression of Hcp proteins in vivo we analyzed titers of antibody against HcpA (HP0211), HcpB (HP0336), HcpC (HP1098), and HcpE (HP0235) in sera from 30 Helicobacter pylori-positive individuals and in a control group of six H. pylori-negative individuals. Significantly higher titers of antibody were observed for H. pylori-positive individuals (P < 0.00005). The highest and lowest titers were observed for HcpC (Δ mean = 1.06) and HcpB (Δ mean = 0.333), respectively. There is a clear correlation among anti-HcpA, -HcpC, and -HcpE immunoglobulin G titers in H. pylori-positive individuals (correlation > 0.7), but there is only a weak correlation for HcpB (correlation < 0.4). These results confirm that Hcp proteins are expressed by H. pylori under natural environmental conditions and that these proteins are recognized by the immune system of the host. The observed correlations are in agreement with the expected distribution of Hcp proteins among H. pylori strains. HcpA, HcpC, and HcpE are present in the genomes of strains 26695 and J99, whereas HcpB is absent from most strains. Since Hcp proteins are specific for H. pylori, immunological assays including Hcp proteins might be of value to detect H. pylori infection and perhaps to distinguish among different groups of H. pylori-positive patients.

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