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Article: Effect of cyclo-oxygenase inhibitors on Helicobacter pylori susceptibility to metronidazole and clarithromycin

TitleEffect of cyclo-oxygenase inhibitors on Helicobacter pylori susceptibility to metronidazole and clarithromycin
Authors
Issue Date2004
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/APT
Citation
Alimentary Pharmacology And Therapeutics, 2004, v. 20 n. 6, p. 675-681 How to Cite?
AbstractBackground: We previously reported that aspirin inhibited Helicobacter pylori growth and suppressed the mutagenic effect of metronidazole. Aim: To determine the effects of a cyclo-oxygenase (COX)-2-specific inhibitor, SC-236, and a non-selective COX inhibitor, indometacin, on the growth, urease activity and antimicrobial susceptibility of H. pylori. Methods: Three H. pylori reference strains, and 18 clinical isolates were treated with SC-236 or indometacin for 24 and 48 h. Growth, urease activity and susceptibility to clarithromycin and metronidazole of the bacteria were assessed by viable colony counting, spectrophotometry and E-test respectively. Results: SC-236 and indometacin inhibited H. pylori growth in a dose-dependent manner with the lowest inhibitory concentrations of 0.03 and 0.1 mM, and the lethal concentrations of 0.09 and 0.3 mM, respectively. The numbers of CFU/mL in Brucella broth containing 0.09 mM SC-236 were 2 log lower at 24 h, and even 3 log lower at 48 h than that at 0 h (P = 0.035, compared with the vehicle control). Treatment of 0.3 mM indometacin reduced the number of CFU/mL by 1 log at 24 h compared with that at 0 h (P = 0.037 compared with the vehicle control). Helicobacter pylori urease activity began to decrease with 0.06 mM SC-236 at 24 h (P = 0.016), and 0.3 mM indometacin at 48 h (P = 0.025). MICs of metronidazole and clarithromycin against H. pylori were decreased significantly in the presence of 0.03 mM SC-236 or 0.1 mM indometacin (all P < 0.001). Conclusion: Both SC-236 and indometacin suppressed the growth and urease activity of H. pylori in a dose-dependent manner, and increased its susceptibility to the antibiotics.
Persistent Identifierhttp://hdl.handle.net/10722/76977
ISSN
2015 Impact Factor: 6.32
2015 SCImago Journal Rankings: 2.833
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorGu, Qen_HK
dc.contributor.authorXia, HHXen_HK
dc.contributor.authorWang, WHen_HK
dc.contributor.authorWang, JDen_HK
dc.contributor.authorWong, WMen_HK
dc.contributor.authorChan, AOOen_HK
dc.contributor.authorYuen, MFen_HK
dc.contributor.authorLam, SKen_HK
dc.contributor.authorCheung, HKLen_HK
dc.contributor.authorLiu, XGen_HK
dc.contributor.authorWong, BCYen_HK
dc.date.accessioned2010-09-06T07:26:57Z-
dc.date.available2010-09-06T07:26:57Z-
dc.date.issued2004en_HK
dc.identifier.citationAlimentary Pharmacology And Therapeutics, 2004, v. 20 n. 6, p. 675-681en_HK
dc.identifier.issn0269-2813en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76977-
dc.description.abstractBackground: We previously reported that aspirin inhibited Helicobacter pylori growth and suppressed the mutagenic effect of metronidazole. Aim: To determine the effects of a cyclo-oxygenase (COX)-2-specific inhibitor, SC-236, and a non-selective COX inhibitor, indometacin, on the growth, urease activity and antimicrobial susceptibility of H. pylori. Methods: Three H. pylori reference strains, and 18 clinical isolates were treated with SC-236 or indometacin for 24 and 48 h. Growth, urease activity and susceptibility to clarithromycin and metronidazole of the bacteria were assessed by viable colony counting, spectrophotometry and E-test respectively. Results: SC-236 and indometacin inhibited H. pylori growth in a dose-dependent manner with the lowest inhibitory concentrations of 0.03 and 0.1 mM, and the lethal concentrations of 0.09 and 0.3 mM, respectively. The numbers of CFU/mL in Brucella broth containing 0.09 mM SC-236 were 2 log lower at 24 h, and even 3 log lower at 48 h than that at 0 h (P = 0.035, compared with the vehicle control). Treatment of 0.3 mM indometacin reduced the number of CFU/mL by 1 log at 24 h compared with that at 0 h (P = 0.037 compared with the vehicle control). Helicobacter pylori urease activity began to decrease with 0.06 mM SC-236 at 24 h (P = 0.016), and 0.3 mM indometacin at 48 h (P = 0.025). MICs of metronidazole and clarithromycin against H. pylori were decreased significantly in the presence of 0.03 mM SC-236 or 0.1 mM indometacin (all P < 0.001). Conclusion: Both SC-236 and indometacin suppressed the growth and urease activity of H. pylori in a dose-dependent manner, and increased its susceptibility to the antibiotics.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/APTen_HK
dc.relation.ispartofAlimentary Pharmacology and Therapeuticsen_HK
dc.rightsAlimentary Pharmacology and Therapeutics. Copyright © Blackwell Publishing Ltd.en_HK
dc.subject.meshAnti-Bacterial Agents - therapeutic useen_HK
dc.subject.meshAnti-Infective Agents - therapeutic useen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshClarithromycin - therapeutic useen_HK
dc.subject.meshCyclooxygenase Inhibitors - therapeutic useen_HK
dc.subject.meshDrug Interactionsen_HK
dc.subject.meshHelicobacter Infections - drug therapyen_HK
dc.subject.meshHelicobacter pylorien_HK
dc.subject.meshHumansen_HK
dc.subject.meshMetronidazole - therapeutic useen_HK
dc.subject.meshPyrazoles - therapeutic useen_HK
dc.subject.meshSulfonamides - therapeutic useen_HK
dc.titleEffect of cyclo-oxygenase inhibitors on Helicobacter pylori susceptibility to metronidazole and clarithromycinen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0269-2813&volume=20&spage=675&epage=681&date=2004&atitle=Effect+of+Cyclo-Oxygenase+Inhibitors+on+Helicobacter+pylori+Susceptibility+to+Metronidazole+and+Clarithromycinen_HK
dc.identifier.emailWang, JD: jidewang@gmail.comen_HK
dc.identifier.emailYuen, MF: mfyuen@hku.hken_HK
dc.identifier.emailWong, BCY: bcywong@hku.hken_HK
dc.identifier.authorityWang, JD=rp00491en_HK
dc.identifier.authorityYuen, MF=rp00479en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1365-2036.2004.02168.xen_HK
dc.identifier.pmid15352916-
dc.identifier.scopuseid_2-s2.0-4644309194en_HK
dc.identifier.hkuros90709en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-4644309194&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume20en_HK
dc.identifier.issue6en_HK
dc.identifier.spage675en_HK
dc.identifier.epage681en_HK
dc.identifier.isiWOS:000223713300011-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridGu, Q=24469982400en_HK
dc.identifier.scopusauthoridXia, HHX=8757161400en_HK
dc.identifier.scopusauthoridWang, WH=23390847100en_HK
dc.identifier.scopusauthoridWang, JD=35309087500en_HK
dc.identifier.scopusauthoridWong, WM=7403972413en_HK
dc.identifier.scopusauthoridChan, AOO=7403167965en_HK
dc.identifier.scopusauthoridYuen, MF=7102031955en_HK
dc.identifier.scopusauthoridLam, SK=7402279800en_HK
dc.identifier.scopusauthoridCheung, HKL=7201839335en_HK
dc.identifier.scopusauthoridLiu, XG=26643623200en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK

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