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Article: Aspirin inhibits the growth of Helicobacter pylori and enhances its susceptibility to antimicrobial agents

TitleAspirin inhibits the growth of Helicobacter pylori and enhances its susceptibility to antimicrobial agents
Authors
Issue Date2003
PublisherBMJ Publishing Group. The Journal's web site is located at http://gut.bmjjournals.com/
Citation
Gut, 2003, v. 52 n. 4, p. 490-495 How to Cite?
AbstractBackground and aim: The role of Helicobacter pylori and aspirin in peptic ulcer formation and recurrence remains an important clinical topic. The interaction between aspirin and H pylori in vitro is also not clear. We investigated the effect of aspirin on the growth of H pylori and on the susceptibility, of H pylori to antimicrobials. Methods: Time killing studies of H pylori were performed with different concentrations of aspirin and salicylate. Growth of bacteria was assessed spectrophotometrically and by viable colony count. The effects of aspirin on the efficiency of colony formation and on metronidazole induced mutation to rifampicin resistance in H pylori were determined. Minimal inhibitory concentrations (MICs) of aspirin and metronidazole were tested by the standard agar dilution method. MICs of amoxycillin and darithromycin were determined by the E test method. Results: Aspirin and salicylate inhibited the growth of H pylori in a dose dependent manner and bactericidal activity was due to cell lysis. Aspirin 400 μg/ml caused a 2 logs decrease in colony forming units/ml at 48 hours, and suppressed the normal ability of metronidazole to induce new mutations to rifampicin. The IC90 of aspirin was 512 μg/ml. Increased susceptibility of amoxycillin, darithromycin, and metronidazole to H pylori was observed at 1 mM (1 80 μg/ml) aspirin. Conclusions: Aspirin inhibited the growth of H pylori, suppressed the mutagenic effect of metronidazole, and enhanced the susceptibility of H pylori to antimicrobial agents. This mechanism is important in future drug development for effective clearing and overcoming resistance.
Persistent Identifierhttp://hdl.handle.net/10722/43100
ISSN
2015 Impact Factor: 14.921
2015 SCImago Journal Rankings: 6.474
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, WHen_HK
dc.contributor.authorWong, WMen_HK
dc.contributor.authorDailidiene, Den_HK
dc.contributor.authorBerg, DEen_HK
dc.contributor.authorGu, Qen_HK
dc.contributor.authorLai, KCen_HK
dc.contributor.authorLam, SKen_HK
dc.contributor.authorWong, BCYen_HK
dc.date.accessioned2007-03-23T04:38:51Z-
dc.date.available2007-03-23T04:38:51Z-
dc.date.issued2003en_HK
dc.identifier.citationGut, 2003, v. 52 n. 4, p. 490-495en_HK
dc.identifier.issn0017-5749en_HK
dc.identifier.urihttp://hdl.handle.net/10722/43100-
dc.description.abstractBackground and aim: The role of Helicobacter pylori and aspirin in peptic ulcer formation and recurrence remains an important clinical topic. The interaction between aspirin and H pylori in vitro is also not clear. We investigated the effect of aspirin on the growth of H pylori and on the susceptibility, of H pylori to antimicrobials. Methods: Time killing studies of H pylori were performed with different concentrations of aspirin and salicylate. Growth of bacteria was assessed spectrophotometrically and by viable colony count. The effects of aspirin on the efficiency of colony formation and on metronidazole induced mutation to rifampicin resistance in H pylori were determined. Minimal inhibitory concentrations (MICs) of aspirin and metronidazole were tested by the standard agar dilution method. MICs of amoxycillin and darithromycin were determined by the E test method. Results: Aspirin and salicylate inhibited the growth of H pylori in a dose dependent manner and bactericidal activity was due to cell lysis. Aspirin 400 μg/ml caused a 2 logs decrease in colony forming units/ml at 48 hours, and suppressed the normal ability of metronidazole to induce new mutations to rifampicin. The IC90 of aspirin was 512 μg/ml. Increased susceptibility of amoxycillin, darithromycin, and metronidazole to H pylori was observed at 1 mM (1 80 μg/ml) aspirin. Conclusions: Aspirin inhibited the growth of H pylori, suppressed the mutagenic effect of metronidazole, and enhanced the susceptibility of H pylori to antimicrobial agents. This mechanism is important in future drug development for effective clearing and overcoming resistance.en_HK
dc.format.extent203125 bytes-
dc.format.extent28672 bytes-
dc.format.extent4936 bytes-
dc.format.mimetypeapplication/pdf-
dc.format.mimetypeapplication/msword-
dc.format.mimetypetext/plain-
dc.languageengen_HK
dc.publisherBMJ Publishing Group. The Journal's web site is located at http://gut.bmjjournals.com/en_HK
dc.relation.ispartofGuten_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsGut. Copyright © B M J Publishing Group.en_HK
dc.subject.meshAnti-bacterial agents - pharmacologyen_HK
dc.subject.meshAspirin - pharmacologyen_HK
dc.subject.meshHelicobacter pylori - drug effects - growth & developmenten_HK
dc.subject.meshDose-response relationship, drugen_HK
dc.subject.meshSalicylates - pharmacologyen_HK
dc.titleAspirin inhibits the growth of Helicobacter pylori and enhances its susceptibility to antimicrobial agentsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0017-5749&volume=52&issue=4&spage=490&epage=495&date=2003&atitle=Aspirin+inhibits+the+growth+of+Helicobacter+pylori+and+enhances+its+susceptibility+to+antimicrobial+agentsen_HK
dc.identifier.emailWong, BCY:bcywong@hku.hken_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1136/gut.52.4.490en_HK
dc.identifier.pmid12631656-
dc.identifier.pmcidPMC1773581-
dc.identifier.scopuseid_2-s2.0-0344405708en_HK
dc.identifier.hkuros80391-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0344405708&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume52en_HK
dc.identifier.issue4en_HK
dc.identifier.spage490en_HK
dc.identifier.epage495en_HK
dc.identifier.isiWOS:000181828100008-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridWang, WH=23390847100en_HK
dc.identifier.scopusauthoridWong, WM=7403972413en_HK
dc.identifier.scopusauthoridDailidiene, D=6506309198en_HK
dc.identifier.scopusauthoridBerg, DE=7202401139en_HK
dc.identifier.scopusauthoridGu, Q=24469982400en_HK
dc.identifier.scopusauthoridLai, KC=7402135595en_HK
dc.identifier.scopusauthoridLam, SK=7402279473en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK

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