The Development of Urease Inhibitors: What Opportunities Exist for Better Treatment of Helicobacter pylori Infection in Children?
Status PubMed-not-MEDLINE Jazyk angličtina Země Švýcarsko Médium electronic
Typ dokumentu časopisecké články
PubMed
28054971
PubMed Central
PMC5296663
DOI
10.3390/children4010002
PII: children4010002
Knihovny.cz E-zdroje
- Klíčová slova
- Helicobacter pylori (H. pylori) infection, children, drug development, pharmacokinetics, urease inhibitors,
- Publikační typ
- časopisecké články MeSH
Stomach infection with Helicobacter pylori (H. pylori) causes severe gastroduodenal diseases in a large number of patients worldwide. The H. pylori infection breaks up in early childhood, persists lifelong if not treated, and is associated with chronic gastritis and an increased risk of peptic ulcers and gastric cancer. In recent years, the problem of drug-resistant strains has become a global concern that makes the treatment more complicated and the infection persistent at higher levels when the antibiotic treatment is stopped. Such problems have led to the development of new strategies to eradicate an H. pylori infection. Currently, one of the most important strategies for the treatment of H. pylori infection is the use of urease inhibitors. Despite the fact that large numbers of molecules have been shown to exert potent inhibitory activity against H. pylori urease, most of them were prevented from being used in vivo and in clinical trials due to their hydrolytic instability, toxicity, and appearance of undesirable side effects. Therefore, it is crucial to focus attention on the available opportunities for the development of urease inhibitors with suitable pharmacokinetics, high hydrolytic stability, and free toxicological profiles. In this commentary, we aim to afford an outline on the current status of the use of urease inhibitors in the treatment of an H. pylori infection, and to discuss the possibility of their development as effective drugs in clinical trials.
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Dolapcioglu C., Koc-Yesiltoprak A., Ahishali E., Kural A., Dolapcioglu H., Soylu A., Dabak R. Sequential therapy versus standard triple therapy in Helicobacter pylori eradication in a high clarithromycin resistance setting. Int. J. Clin. Exp. Med. 2014;7:2324–2328. PubMed PMC
Go M.F. Review article: Natural history and epidemiology of Helicobacter pylori infection. Aliment. Pharmacol. Ther. 2002;16:S3–S15. doi: 10.1046/j.1365-2036.2002.0160s1003.x. PubMed DOI
Izzotti A., Durando P., Ansaldi F., Gianiorio F., Pulliero A. Interaction between Helicobacter pylori, diet, and genetic polymorphisms as related to non-cancer diseases. Mutat. Res. 2009;667:142–157. doi: 10.1016/j.mrfmmm.2009.02.002. PubMed DOI
Kawakami E., Machado R.S., Ogata S.K., Langner M. Decrease in prevalence of Helicobacter pylori infection during a 10-year period in Brazilian children. Arq. Gastroenterol. 2008;45:147–151. doi: 10.1590/S0004-28032008000200011. PubMed DOI
Kusters J.G., van Vliet A.H., Kuipers E.J. Pathogenesis of Helicobacter pylori infection. Clin. Microbiol. Rev. 2006;19:449–490. doi: 10.1128/CMR.00054-05. PubMed DOI PMC
Ferreira J., Moss S.F. Current Paradigm and Future Directions for Treatment of Helicobacter pylori Infection. Curr. Treat. Options Gastroenterol. 2014;12:373–384. doi: 10.1007/s11938-014-0027-6. PubMed DOI
Essa A.S., Kramer J.R., Graham D.Y., Treiber G. Meta-analysis: Four-drug, three-antibiotic, non-bismuth-containing “concomitant therapy” versus triple therapy for Helicobacter pylori eradication. Helicobacter. 2009;14:109–118. doi: 10.1111/j.1523-5378.2009.00671.x. PubMed DOI PMC
Hassan S.T.S., Majerová M., Šudomová M., Berchová K. Antibacterial activity of natural compounds—essential oils. Ceska Slov. Farm. 2015;64:243–253. PubMed
Modlin I.M. From Prout to the proton pump—A history of the science of gastric acid secretion and the surgery of peptic ulcer. Surg. Gynecol. Obstet. 1990;170:81–96. PubMed
Gehlot V., Mahant S., Mukhopadhyay A.K., Das K., De R., Kar P., Das R. Antimicrobial susceptibility profiles of Helicobacter pylori isolated from patients in North India. J. Glob. Antimicrob. Resist. 2016;5:51–56. doi: 10.1016/j.jgar.2015.09.009. PubMed DOI
Chaabane N.B., Al-Adhba H.S. Ciprofloxacin-containing versus clarithromycin-containing sequential therapy for Helicobacter pylori eradication: A randomized trial. Indian J. Gastroenterol. 2015;34:68–72. doi: 10.1007/s12664-015-0535-x. PubMed DOI
Boer de W.A., Guido N., Tytgat J. Regular review: Treatment of Helicobacter pylori infection. Br. Med. J. 2000;320:31–34. doi: 10.1136/bmj.320.7226.31. PubMed DOI PMC
Mansour-Ghanaei F., Joukar F., Mojtahedi K., Sokhanvar H., Askari K., Shafaeizadeh A. Does treatment of Helicobacter pylori infection reduce gastric precancerous lesions? Asian Pac. J. Cancer Prev. 2015;16:1571–1574. doi: 10.7314/APJCP.2015.16.4.1571. PubMed DOI
Nagahara A., Miwa H., Ogawa K., Kurosawa A., Ohkura R., Iida N., Sato N. Addition of metronidazole to rabeprazole-amoxicillin-clarithromycin regimen for Helicobacter pylori infection provides an excellent cure rate with five-day therapy. Helicobacter. 2000;5:88–93. doi: 10.1046/j.1523-5378.2000.00013.x. PubMed DOI
Bartnik W. Clinical aspects of Helicobacter pylori infection. Pol. Arch. Med. Wewn. 2008;118:426–430. PubMed
O’Connor A., Vaira D., Gisbert J.P., O’Morain C. Treatment of Helicobacter pylori infection 2014. Helicobacter. 2014;19(Suppl. 1):38–45. doi: 10.1111/hel.12163. PubMed DOI
Hassan S.T.S., Berchová K., Majerová M., Pokorná M., Švajdlenka E. In vitro synergistic effect of Hibiscus sabdariffa aqueous extract in combination with standard antibiotics against Helicobacter pylori clinical isolates. Pharm. Biol. 2016;54:1736–1740. doi: 10.3109/13880209.2015.1126618. PubMed DOI
Benini S., Rypniewski W.R., Wilson K.S., Miletti S., Ciurli S., Mangani S. A new proposal for urease mechanism based on the crystal structures of the native and inhibited enzyme from Bacillus pasteurii: Why urea hydrolysis costs two nickels. Structure. 1999;7:205–216. doi: 10.1016/S0969-2126(99)80026-4. PubMed DOI
Benini S., Rypniewski W.R., Wilson K.S., Mangani S., Ciurli S. Molecular details of urease inhibition by boric acid: insights into the catalytic mechanism. J. Am. Chem. Soc. 2004;126:3714–3715. doi: 10.1021/ja049618p. PubMed DOI
Kosikowska P., Berlicki Ł. Urease inhibitors as potential drugs for gastric and urinary tract infections: A patent review. Expert Opin. Ther. Pat. 2011;21:945–957. doi: 10.1517/13543776.2011.574615. PubMed DOI
Adu-Aryee N.A., Aabakken L., Dedey F., Nsaful J., Kudzi W. Comparison of endoscopic based diagnosis with Helicobacter urease test for Helicobacter pylori infection. BMC Res. Notes. 2016;9:421. doi: 10.1186/s13104-016-2237-6. PubMed DOI PMC
Macegoniuk K., Grela E., Palus J., Rudzińska-Szostak E., Grabowiecka A., Biernat M., Berlicki Ł. 1,2-Benzisoselenazol-3(2H)-one Derivatives As a New Class of Bacterial Urease Inhibitors. J. Med. Chem. 2016;59:8125–8133. doi: 10.1021/acs.jmedchem.6b00986. PubMed DOI
Stingl K., Sltendorf K., Bakker E.P. Acid survival of Helicobacter pylori: How does urease activity trigger cytoplasmic pH homeostasis? Trends Microbiol. 2002;10:70–74. doi: 10.1016/S0966-842X(01)02287-9. PubMed DOI
Weeks D.L., Eskandari S., Scott D.R., Sachs G. A H+-gated urea channel: The link between Helicobacter pylori urease and gastric colonization. Science. 2000;287:482–485. doi: 10.1126/science.287.5452.482. PubMed DOI
Krishnamurthy P., Parlow M., Zitzer J.B., Vakil N.B., Mobley H.L., Levy M., Phadnis S.H., Dunn B.E. Helicobacter pylori containing only cytoplasmic urease is susceptible to acid. Infect. Immun. 1998;66:5060–5066. PubMed PMC
Evans D.J., Jr., Evans D.G., Kirkpatrick S.S., Graham D.Y. Characterization of the Helicobacter pylori urease and purification of its subunits. Microb. Pathog. 1991;10:15–26. doi: 10.1016/0882-4010(91)90062-F. PubMed DOI
Ha N.C., Oh S.T., Sung J.Y., Cha K.A., Lee M.H., Oh B.H. Supramolecular assembly and acid resistance of Helicobacter pylori urease. Nat. Struct. Biol. 2001;8:505–509. doi: 10.1038/88563. PubMed DOI
Khan S., Karim A., Iqbal S. Helicobacter urease: Niche construction at the single molecule level. J. Biosci. 2009;34:503–511. doi: 10.1007/s12038-009-0069-4. PubMed DOI
Park I.S., Hausinger R.P. Evidence for the presence of urease apoprotein complexes containing UreD, UreF, and UreG in cells that are competent for in vivo enzyme activation. J. Bacteriol. 1995;177:1947–1951. doi: 10.1128/jb.177.8.1947-1951.1995. PubMed DOI PMC
Hu L.T., Foxall P.A., Russell R., Mobley H.L. Purification of recombinant Helicobacter pylori urease apoenzyme encoded by ureA and ureB. Infect. Immun. 1992;60:2657–2666. PubMed PMC
Zerner B. Recent advances in the chemistry of an old enzyme, urease. Bioorg. Chem. 1991;19:116–131. doi: 10.1016/0045-2068(91)90048-T. DOI
Rektorschek M., Buhmann A., Weeks D., Schwan D., Bensch K.W., Eskandari S., Scott D., Sachs G., Melchers K. Acid resistance of Helicobacter pylori depends on the UreI membrane protein and an inner membrane proton barrier. Mol. Microb. 2000;36:141–152. doi: 10.1046/j.1365-2958.2000.01835.x. PubMed DOI
Scott D.R., Marcus E.A., Weeks D.L., Lee A., Melchers K., Sachs G. Expression of the Helicobacter pylori ureI gene is required for acidic pH activation of cytoplasmic urease. Infect. Immun. 2000;68:470–477. doi: 10.1128/IAI.68.2.470-477.2000. PubMed DOI PMC
Hassan S.T.S., Žemlička M. Plant-Derived Urease Inhibitors as Alternative Chemotherapeutic Agents. Arch. Pharm. (Weinh.) 2016;349:507–522. doi: 10.1002/ardp.201500019. PubMed DOI
Matongo F., Nwodo U.U. In vitro assessment of Helicobacter pylori ureases inhibition by honey fractions. Arch. Med. Res. 2014;45:540–546. doi: 10.1016/j.arcmed.2014.09.001. PubMed DOI
Palizban A., Saghaie L. Synthesis and evaluation of the complex-forming ability of hydroxypyranones and hydroxypyridinones with Ni (II) as possible inhibitors for urease enzyme in Helicobacter pylori. Res. Pharm. Sci. 2016;11:332–342. doi: 10.4103/1735-5362.189319. PubMed DOI PMC
Modolo L.V., de Souza A.X., Horta L.P., Araujo D.P., de Fátima Â. An overview on the potential of natural products as ureases inhibitors: A review. J. Adv. Res. 2015;6:35–44. doi: 10.1016/j.jare.2014.09.001. PubMed DOI PMC
Follmer C. Ureases as a target for the treatment of gastric and urinary infections. J. Clin. Pathol. 2010;63:424–430. doi: 10.1136/jcp.2009.072595. PubMed DOI
Jain S.K., Haider T., Kumar A., Jain A. Lectin-Conjugated Clarithromycin and Acetohydroxamic Acid-Loaded PLGA Nanoparticles: A Novel Approach for Effective Treatment of H. pylori. AAPS PharmSciTech. 2016;17:1131–1140. doi: 10.1208/s12249-015-0443-5. PubMed DOI
Umamaheshwari R.B., Jain N.K. Receptor-mediated targeting of lipobeads bearing acetohydroxamic acid for eradication of Helicobacter pylori. J. Control. Release. 2004;99:27–40. doi: 10.1016/j.jconrel.2004.06.006. PubMed DOI
Griffith D.P. Urease stones. Urol. Res. 1979;7:215–221. doi: 10.1007/BF00257208. PubMed DOI