You are on page 1of 2

10/15/2014

PotentialdrugthatcouldhelptreatcysticfibrosisidentifiedbyresearchersScienceDaily

Potentialdrugthatcouldhelptreatcysticfibrosisidentifiedby
researchers
Date:

October14,2014

Source: eLife
Byscreeningover2,000approveddrugsandnaturalproducts,scientistshaveshownthattannicacidmayhelpease
theimpactofbacteriallunginfectionsincysticfibrosispatients.Testscompletedusingexperimentallymodifiedfrog
oocytesshowthattannicacidcounteractstheharmfuleffectofanenzymeproducedbythebacteriumStaphylococcus
aureus(S.aureus).However,moreresearchisneededtofindoutiftannicacidcanhelptreatS.aureusinfectionsin
humans.
Fromanearlyage,thelungsofindividualswithcysticfibrosis(CF)arecolonisedandinfectedbybacteria,acommon
examplebeingS.aureus.Thesebacterialinfectionscausethelungstobecomeinflamed,infected,andcaneventually
leadtopermanentlungdamage.ResearchersfromtheUniversityofPennsylvaniaandtheHowardHughesMedical
InstitutepreviouslyshowedthatanenzymecalledSphingomyelinphosphodiesteraseC(SMaseC)producedbytheS.
aureusbacteriummayharmthehealthofCFpatients.Now,theyhavediscoveredaninhibitorforthispathogenic
bacterialenzyme.
InpatientssufferingfromCF,thecysticfibrosis"transmembraneconductanceregulator"(CFTR)channelsarefaulty,
causingathickmucustobuildupintheirlungs.Intheseexperiments,theauthorsusedoocytesfromtheXenopus
typeoffrogthathadbeengeneticallymodifiedtoexpressCFTRchannelsontheircellsurfacetomeasurethe
effectthatSMaseChasonCFTRchannels.TheysawthattheSMaseCenzymesuppressesCFTRchannelactivityin
theseexperimentallymodifiedfrogoocytes,andalsoinahumanlungcellline.
TheseresultssuggestthattheSMaseCenzyme,producedbytheS.aureasbacterium,mayreduceanyresidual
channelactivityinCFpatients.TheproblemsoriginatingfromgeneticdefectsinCFTRchannelsarelikelymadegreater
iftheenzymereducesthefunctionoftheCFTRchannelevenfurther.
SMaseCalsosuppressesatypeofvoltagegatedpotassiumchannel,knownastheKv1.3channel,inimmunecells.
Suppressionofthesepotassiumchannelsisknowntoweakenhostimmunity,whichwouldmakeitmoredifficultforthe
CFpatientstorecoverfromlunginfections.
Totryandcounteracttheeffectsoftheenzyme,theresearcherswentontotestacollectionofapproveddrugsand
naturalproductsinachemicallibrary.Theyfoundthattannicacidareadilyavailableandinexpensivenaturalproduct
thathasbeenusedtotreatdiseaseasfarbackas1850stoppedSMaseCfromhavinganegativeeffectonboththe
CFTRandtheKv1.3channels."WehopetotestwhethertheapplicationoftheSMaseCinhibitortannicacid,in
conjunctionwitheffectiveantibiotictreatmentandsupportivemeasures,willprovideasignificanttherapeutic
improvementovercurrenttreatmentsforcysticfibrosis,"Dr.ZheLu,theseniorauthor,says.Histeamisalsoworking
hardtounderstandtheexactmechanismbywhichtannicacidcountersthenegativeactionsofSMaseC.
StorySource:
TheabovestoryisbasedonmaterialsprovidedbyeLife.Note:Materialsmaybeeditedforcontentandlength.
JournalReference:
1. YajamanaRamu,YanpingXu,HyeonGyuShin,ZheLu.CounteractingsuppressionofCFTRandvoltagegated
Kchannelsbyabacterialpathogenicfactorwiththenaturalproducttannicacid.eLife,20143DOI:
10.7554/eLife.03683
CiteThisPage:
MLA

APA

Chicago

http://www.sciencedaily.com/releases/2014/10/141014152538.htm

1/2

10/15/2014

PotentialdrugthatcouldhelptreatcysticfibrosisidentifiedbyresearchersScienceDaily

eLife."Potentialdrugthatcouldhelptreatcysticfibrosisidentifiedbyresearchers."ScienceDaily.ScienceDaily,14
October2014.<www.sciencedaily.com/releases/2014/10/141014152538.htm>.

http://www.sciencedaily.com/releases/2014/10/141014152538.htm

2/2

You might also like