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Article: Chlamydia trachomatis infection increases fallopian tube PROKR2 via TLR2 and NFκB activation resulting in a microenvironment predisposed to ectopic pregnancy

TitleChlamydia trachomatis infection increases fallopian tube PROKR2 via TLR2 and NFκB activation resulting in a microenvironment predisposed to ectopic pregnancy
Authors
Issue Date2011
PublisherAmerican Society for Investigative Pathology. The Journal's web site is located at http://www.amjpathol.org
Citation
American Journal Of Pathology, 2011, v. 178 n. 1, p. 253-260 How to Cite?
AbstractChlamydia trachomatis and smoking are major risk factors for tubal ectopic pregnancy (EP), but the underlying mechanisms of these associations are not completely understood. Fallopian tube (FT) from women with EP exhibit altered expression of prokineticin receptors 1 and 2 (PROKR1 and PROKR2); smoking increases FT PROKR1, resulting in a micro-environment predisposed to EP. We hypothesize that C. trachomatis also predisposes to EP by altering FT PROKR expression and have investigated this by examining NFκB activation via ligation of the Toll-like receptor (TLR) family of cell-surface pattern recognition receptors. PROKR2 mRNA was higher in FT from women with evidence of past C. trachomatis infection than in those without (P < 0.05), and was also increased in FT explants and in oviductal epithelial cell line OE-E6/E7 infected with C. trachomatis (P < 0.01) or exposed to UV-killed organisms (P < 0.05). The ability of both live and dead organisms to induce this effect suggests ligation of a cell-surface-expressed receptor. FT epithelium and OE-E6/E7 were both found to express TLR2 and TLR4 by immunohistochemistry. Transfection of OE-E6/E7 cells with dominant-negative TLR2 or IκBα abrogated the C. trachomatis-induced PROKR2 expression. We propose that ligation of tubal TLR2 and activation of NFκB by C. trachomatis leads to increased tubal PROKR2, thereby predisposing the tubal microenvironment to ectopic implantation. Copyright © 2011 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/139904
ISSN
2015 Impact Factor: 4.206
2015 SCImago Journal Rankings: 2.653
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Wellbeing of Women ProjectRG993
Medical Research Council (MRC)U.1276.00.004.00002.02
Scottish Government Rural and Environmental Research and Analysis Directorate (RERAD)
Funding Information:

This work was supported by a Wellbeing of Women Project Grant (RG993) (A.W.H., H.N.J., G.E., H.O.D.C.). H.N.J. was supported by Medical Research Council (MRC) core funding (U.1276.00.004.00002.02). G.E. was funded by the Scottish Government Rural and Environmental Research and Analysis Directorate (RERAD). A.W.H. is supported by an MRC Clinician Scientist Fellowship.

References

 

DC FieldValueLanguage
dc.contributor.authorShaw, JLVen_HK
dc.contributor.authorWills, GSen_HK
dc.contributor.authorLee, KFen_HK
dc.contributor.authorHorner, PJen_HK
dc.contributor.authorMcClure, MOen_HK
dc.contributor.authorAbrahams, VMen_HK
dc.contributor.authorWheelhouse, Nen_HK
dc.contributor.authorJabbour, HNen_HK
dc.contributor.authorCritchley, HODen_HK
dc.contributor.authorEntrican, Gen_HK
dc.contributor.authorHorne, AWen_HK
dc.date.accessioned2011-09-23T05:59:59Z-
dc.date.available2011-09-23T05:59:59Z-
dc.date.issued2011en_HK
dc.identifier.citationAmerican Journal Of Pathology, 2011, v. 178 n. 1, p. 253-260en_HK
dc.identifier.issn0002-9440en_HK
dc.identifier.urihttp://hdl.handle.net/10722/139904-
dc.description.abstractChlamydia trachomatis and smoking are major risk factors for tubal ectopic pregnancy (EP), but the underlying mechanisms of these associations are not completely understood. Fallopian tube (FT) from women with EP exhibit altered expression of prokineticin receptors 1 and 2 (PROKR1 and PROKR2); smoking increases FT PROKR1, resulting in a micro-environment predisposed to EP. We hypothesize that C. trachomatis also predisposes to EP by altering FT PROKR expression and have investigated this by examining NFκB activation via ligation of the Toll-like receptor (TLR) family of cell-surface pattern recognition receptors. PROKR2 mRNA was higher in FT from women with evidence of past C. trachomatis infection than in those without (P < 0.05), and was also increased in FT explants and in oviductal epithelial cell line OE-E6/E7 infected with C. trachomatis (P < 0.01) or exposed to UV-killed organisms (P < 0.05). The ability of both live and dead organisms to induce this effect suggests ligation of a cell-surface-expressed receptor. FT epithelium and OE-E6/E7 were both found to express TLR2 and TLR4 by immunohistochemistry. Transfection of OE-E6/E7 cells with dominant-negative TLR2 or IκBα abrogated the C. trachomatis-induced PROKR2 expression. We propose that ligation of tubal TLR2 and activation of NFκB by C. trachomatis leads to increased tubal PROKR2, thereby predisposing the tubal microenvironment to ectopic implantation. Copyright © 2011 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.en_HK
dc.languageengen_US
dc.publisherAmerican Society for Investigative Pathology. The Journal's web site is located at http://www.amjpathol.orgen_HK
dc.relation.ispartofAmerican Journal of Pathologyen_HK
dc.subject.meshChlamydia Infections - complications - pathologyen_US
dc.subject.meshChlamydia trachomatisen_US
dc.subject.meshFallopian Tubes - metabolism - microbiology - pathologyen_US
dc.subject.meshNF-kappa B - metabolismen_US
dc.subject.meshPregnancy, Ectopic - metabolism - microbiology - pathologyen_US
dc.titleChlamydia trachomatis infection increases fallopian tube PROKR2 via TLR2 and NFκB activation resulting in a microenvironment predisposed to ectopic pregnancyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0002-9440&volume=178&issue=1&spage=253&epage=260&date=2011&atitle=Chlamydia+trachomatis+infection+increases+fallopian+tube+PROKR2+via+TLR2+and+NFκB+activation+resulting+in+a+microenvironment+predisposed+to+ectopic+pregnancyen_US
dc.identifier.emailLee, KF:ckflee@hku.hken_HK
dc.identifier.authorityLee, KF=rp00458en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1016/j.ajpath.2010.11.019en_HK
dc.identifier.pmid21224062-
dc.identifier.pmcidPMC3016599en_US
dc.identifier.scopuseid_2-s2.0-79251482778en_HK
dc.identifier.hkuros196017en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79251482778&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume178en_HK
dc.identifier.issue1en_HK
dc.identifier.spage253en_HK
dc.identifier.epage260en_HK
dc.identifier.isiWOS:000286493700028-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridShaw, JLV=7403899035en_HK
dc.identifier.scopusauthoridWills, GS=26649318200en_HK
dc.identifier.scopusauthoridLee, KF=26643097500en_HK
dc.identifier.scopusauthoridHorner, PJ=35595911800en_HK
dc.identifier.scopusauthoridMcClure, MO=16186017600en_HK
dc.identifier.scopusauthoridAbrahams, VM=7003513827en_HK
dc.identifier.scopusauthoridWheelhouse, N=16044431200en_HK
dc.identifier.scopusauthoridJabbour, HN=7005209265en_HK
dc.identifier.scopusauthoridCritchley, HOD=7006731536en_HK
dc.identifier.scopusauthoridEntrican, G=7003339226en_HK
dc.identifier.scopusauthoridHorne, AW=8067885000en_HK

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