scholarly journals Idebenone Acts against Growth of Helicobacter pylori by Inhibiting Its Respiration

2006 ◽  
Vol 50 (6) ◽  
pp. 2237-2239 ◽  
Author(s):  
Sakiko Inatsu ◽  
Ayumi Ohsaki ◽  
Kumiko Nagata
Keyword(s):  
Helicobacter Pylori ◽  
Coenzyme Q ◽  
Atp Level ◽  
Respiratory Inhibition ◽  
Low Concentrations ◽  
H Pylori

ABSTRACT Growth of Helicobacter pylori was inhibited by the quinones, idebenone, duroquinone, menadione, juglone, and coenzyme Q1 at low concentrations of 0.8 to 3.2 μg/ml. Idebenone specifically inhibited H. pylori growth by inhibiting respiration and decreasing the cellular ATP level. The respiratory inhibition was accompanied by reduction of idebenone by the H. pylori cells.

scholarly journals Mouse-Colonizing Helicobacter pylori SS1 Is Unusually Susceptible to Metronidazole Due to Two Complementary Reductase Activities

2000 ◽  
Vol 44 (11) ◽  
pp. 3127-3132 ◽  
Author(s):  
Jin-Yong Jeong ◽  
Douglas E. Berg
Keyword(s):  
Helicobacter Pylori ◽  
Kanamycin Resistance ◽  
Phenotypic Traits ◽  
Insertion Mutant ◽  
Low Concentrations ◽  
Mutant Strains ◽  
Resistance Markers ◽  
Clinically Significant ◽  
H Pylori ◽  
Derivatives Of

ABSTRACT In most strains of Helicobacter pylori, mutational inactivation of the rdxA (HP0954) gene, which encodes a nitroreductase that converts metronidazole (MTZ) from a harmless prodrug to a mutagenic and bacteriocidal product, is sufficient to make this pathogen resistant to clinically significant levels of MTZ. Here we report that SS1, a strain with the special ability to colonize mice, is unusual in being susceptible to very low concentrations of MTZ (0.5 μg/ml) and in being especially difficult to mutate to MTZ resistance (Mtzr). These phenotypic traits were traced to expression in this strain of the normally quiescent H. pylori frxAgene (HP0642, an rdxA paralog) along with rdxA. Transformation tests using rdxA::camand frxA::kan insertion mutant DNAs, with selection solely for the chloramphenicol and kanamycin resistance markers, and sequence analyses of frxA in spontaneous Mtzr derivatives of rdxA null mutant strains each showed that the development of Mtzr in SS1 required inactivation of both rdxA and frxA. Inactivation of either gene alone left SS1 susceptible to MTZ, although it was readily mutable from an MTZ-susceptible to an Mtzrphenotype. Reverse transcriptase PCR tests showed that frxAmRNA was at least 10-fold more abundant in SS1 than in reference strain 26695. It is proposed that these reductases play primarily nutritional roles during bacterial growth.

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 Effect of Chlorine on Incorporation of Helicobacter pylori into Drinking Water Biofilms

2009 ◽  
Vol 76 (5) ◽  
pp. 1669-1673 ◽  
Author(s):  
M. S. Gi�o ◽  
N. F. Azevedo ◽  
S. A. Wilks ◽  
M. J. Vieira ◽  
C. W. Keevil
Keyword(s):  
Helicobacter Pylori ◽  
Drinking Water ◽  
Nucleic Acid ◽  
Pure Culture ◽  
Peptide Nucleic Acid ◽  
Culture Methods ◽  
Low Concentrations ◽  
H Pylori ◽  
Specific Peptide ◽  
Effect Of Chlorine

ABSTRACT The use of a specific peptide nucleic acid (PNA) probe demonstrated that Helicobacter pylori persisted inside biofilms exposed to low concentrations of chlorine (0.2 and 1.2 mg liter−1) for at least 26 days, although no culturable cells were recovered. Coupled with data obtained using viability stains in pure culture, this result suggests that H. pylori can survive chlorination but remain undetectable by culture methods, which can be effectively replaced by PNA hybridization.

scholarly journals SpoT-mediated NapA upregulation promotes oxidative stress-induced Helicobacter pylori biofilm formation and confers multidrug resistance

2021 ◽  
Author(s):  
Yican Zhao ◽  
Yuying Cai ◽  
Zhenghong Chen ◽  
Huanjie Li ◽  
Zhengzheng Xu ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Multidrug Resistance ◽  
Biofilm Formation ◽  
Drug Resistant ◽  
Low Concentrations ◽  
Target Molecules ◽  
H Pylori ◽  
Insight Into

Recently, there is increased incidence of drug-resistant Helicobacter pylori infection. Biofilm formation confers multidrug resistance to bacteria. Moreover, it has been found that the formation of biofilm on the surface of gastric mucosa is an important reason for the difficulty of eradication of H. pylori. The mechanisms underlying H. pylori biofilm formation in vivo have not been elucidated. Reactive oxygen species (ROS) released by the host immune cells in response to H. pylori infection cannot effectively clear the pathogen. Moreover, the extracellular matrix of the biofilm protects the bacteria against ROS-mediated toxicity. This study hypothesized that ROS can promote H. pylori biofilm formation and treatment with low concentrations of hydrogen peroxide (H2O2) promoted this process in vitro. The comparative transcriptome analysis of planktonic and biofilm-forming cells revealed that the expression of SpoT, a (p)ppGpp (guanosine 3'-diphosphate 5'-triphosphate and guanosine 3',5'-bispyrophosphate) synthetase/hydrolase, is upregulated in H2O2-induced biofilms and that knockout of spoT inhibited H. pylori biofilm formation. Additionally, this study examined the key target molecules involved in SpoT regulation using weighted gene co-expression network analysis. The analysis revealed that neutrophil-activating protein (NapA; HP0243) promoted H2O2-induced biofilm formation and conferred multidrug resistance. Furthermore, vitamin C exhibited anti-H. pylori biofilm activity and downregulated the expression of napA in vitro. These findings provide novel insight into the clearance of H. pylori biofilms.

scholarly journals Anti-Helicobacter Pylori Activity of Four Alchemilla Species (Rosaceae)

2015 ◽  
Vol 10 (8) ◽  
pp. 1934578X1501000 ◽  
Author(s):  
Marija Krivokuća ◽  
Marjan Niketić ◽  
Marina Milenković ◽  
Nataša Golić ◽  
Carla Masia ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Ellagic Acid ◽  
Reference Strain ◽  
Clinical Isolates ◽  
Strain Atcc ◽  
Strong Activity ◽  
Methanol Extracts ◽  
Low Concentrations ◽  
Significant Difference ◽  
H Pylori

The present study evaluated the anti- Helicobacter pylori activity of Alchemilla glabra Neygenf. ( A. sect. Alchemilla), A. monticola Opiz ( A. sect. Plicatae S.E. Fröhner), A. fissa Günther & Schummel ( A. sect. Calycinae (Buser) Buser) and A. viridiflora Rothm. ( A. sect. Calycinae), and identified ellagic acid and quercetin-3- O-β-D-glucoside. Anti- H. pylori activity was tested against ten clinical isolates and one reference strain (ATCC 43504). The methanol extracts were more active than the dichloromethane and cyclohexane extracts. The ranges of concentrations were between 4 μg/mL for methanol extracts of A. viridiflora, A. glabra and A. monticola, and 256 μg/mL for cyclohexane extracts of A. viridiflora, A. glabra and A. fissa. The best overall activity was obtained with A. monticola extracts. No significant difference was found in the ellagic acid contents of the methanol extracts of the tested Alchemilla species (0.2–0.3 mg/mL), and anti- H. pylori activity was similar (4–32 μg/mL). Ellagic acid exhibited strong activity at very low concentrations (0.125–0.5 μg/mL), while the second identified compound, quercetin-3- O-β-D-glucoside, was also very active in concentration of 2–16 μg/mL.

l-Serine, d- and l-proline and alanine as respiratory substrates of Helicobacter pylori: correlation between in vitro and in vivo amino acid levels

Microbiology ◽  
2003 ◽  
Vol 149 (8) ◽  
pp. 2023-2030 ◽  
Author(s):  
Kumiko Nagata ◽  
Yoko Nagata ◽  
Tadashi Sato ◽  
Masayuki A. Fujino ◽  
Kazuhiko Nakajima ◽  
...  
Keyword(s):  
Amino Acids ◽  
Helicobacter Pylori ◽  
Oxygen Uptake ◽  
Energy Sources ◽  
Whole Cells ◽  
Low Concentrations ◽  
Amino Acid Levels ◽  
H Pylori

Helicobacter pylori whole cells showed high rates of oxygen uptake with l-serine and l-proline as respiratory substrates, and somewhat lower rates with d-alanine and d-proline. These respiratory activities were inhibited by rotenone and antimycin A at low concentrations. Since pyruvate was produced from l-serine and d- and l-alanine in whole cells, the respiratory activities with these amino acids as substrates occurred via pyruvate. Whole cells showed 2,6-dichlorophenolindophenol (DCIP)-reducing activities with d- and l-proline and d-alanine as substrates, suggesting that hydrogen removed from these amino acids also participated in oxygen uptake by the whole cells. High amounts of l-proline, d- and l-alanine, and l-serine were present in H. pylori cells, and these amino acids also predominated in samples of human gastric juice. H. pylori seems to utilize d- and l-proline, d-alanine and l-serine as important energy sources in its habitat of the mucous layer of the stomach.

scholarly journals Antibacterial action of acriflavine hydrochloride for eradication of the gastric pathogen Helicobacter pylori

2020 ◽  
Vol 367 (21) ◽  
Author(s):  
Ankita Tehlan ◽  
Bipul Chandra Karmakar ◽  
Sangita Paul ◽  
Raghwan Kumar ◽  
Inderjeet Kaur ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Synergistic Effect ◽  
Clinical Isolates ◽  
The Novel ◽  
Mice Model ◽  
Antibiotic Resistant ◽  
Low Concentrations ◽  
H Pylori

ABSTRACT Helicobacter pylori, a type 1 carcinogen, accounts for numerous gastric cancer-related deaths worldwide. Repurposing existing drugs or developing new ones for a combinatorial approach against increasing antimicrobial resistance is the need of the hour. This study highlights the efficacy of acriflavine hydrochloride (ACF-HCl) in inhibiting the growth of H. pylori reference strain and antibiotic-resistant clinical isolates at low concentrations. ACF-HCl inhibits H. pylori growth at MIC value 10 times less than that in Escherichia coli, another Gram-negative bacteria. Furthermore, ACF-HCl demonstrates synergistic effect with clarithromycin, a commonly used antibiotic against H. pylori. ACF-HCl treatment also eradicates H. pylori infection in the mice model efficiently. Our in vitro data indicate that bacterial membrane is the prime target. The novel action of ACF-HCl against antibiotic-resistant clinical isolates, synergistic effect with the conventional antibiotic clarithromycin and eradication of H. pylori from infected mice highlight the potential of ACF-HCl as a promising therapeutic agent against H. pylori by itself as well as for combinatorial therapy.

The rod-to-coccoid body transformation in cultures of Helicobacter pylori

1990 ◽  
Vol 48 (3) ◽  
pp. 626-627
Author(s):  
A. R. Crooker ◽  
W. G. Kraft ◽  
T. L. Beard ◽  
M. C. Myers
Keyword(s):  
Helicobacter Pylori ◽  
Growth Cycle ◽  
Negative Bacterium ◽  
Body Formation ◽  
Coccoid Form ◽  
Spiral Form ◽  
Prolonged Culture ◽  
H Pylori ◽  
Upper Gastrointestinal

Helicobacter pylori is a microaerophilic, gram-negative bacterium found in the upper gastrointestinal tract of humans. There is strong evidence that H. pylori is important in the etiology of gastritis; the bacterium may also be a major predisposing cause of peptic ulceration. On the gastric mucosa, the organism exists as a spiral form with one to seven sheathed flagella at one (usually) or both poles. Short spirals were seen in the first successful culture of the organism in 1983. In 1984, Marshall and Warren reported a coccoid form in older cultures. Since that time, other workers have observed rod and coccal forms in vitro; coccoid forms predominate in cultures 3-7 days old. We sought to examine the growth cycle of H. pylori in prolonged culture and the mode of coccoid body formation.

Peptische Ulzera und Helicobacter pylori: Wie wir wissen, was wir wissen

2015 ◽  
Vol 72 (7) ◽  
pp. 475-480
Author(s):  
Raphael Scholl
Keyword(s):  
Helicobacter Pylori ◽  
Kontrollierte Studie ◽  
H Pylori ◽  
Peptische Ulzera

Zusammenfassung. Zu den wichtigsten Ursachen peptischer Ulzera gehört das Bakterium Helicobacter pylori. Aber wie wurde dieser ursächliche Zusammenhang nachgewiesen? Aufschluss darüber gibt die Geschichte und Theorie einer Reihe einschlägiger Studien, die in den 1980er Jahren durchgeführt wurden. Am Anfang stand die Entdeckung einer blossen Korrelation zwischen dem neu entdeckten Bakterium und peptischen Ulzera in Magenbiopsien. Unklar blieb, ob das Bakterium die Krankheit verursachte, oder ob es bloss eine opportunistische bakterielle Besiedlung darstellte. Ohne Tiermodell war der experimentelle Nachweis der Richtung der Verursachung jedoch schwierig: Zwar wurde in einem couragierten Selbstversuch mit einer geschluckten Bakterienkultur eine Gastritis beobachtet – aber der Einzelfall war wenig aussagekräftig. Die Schwächen des Selbstversuchs liessen sich durch eine randomisierte, Plazebo-kontrollierte Studie beheben, die den Anforderungen des dritten Koch’schen Postulats gerecht wurde. Darüber hinaus war es notwendig, erste Aufschlüsse über den Mechanismus der ursächlichen Verbindung zwischen H. pylori und peptischen Ulzera zu gewinnen: Wie zum Beispiel kann das Bakterium im sauren Milieu des Magens überleben? Die wissenschaftshistorische und wissenschaftstheoretische Betrachtung des Falls illustriert, wie medizinisches Wissen schrittweise aufgebaut wird.

Sign in / Sign up

Export Citation Format

Share Document