Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/106438
Type: Artigo de periódico
Title: Tlr2-mediated Cell Stimulation In Bacterial Vaginosis
Author: Mares D.
Simoes J.A.
Novak R.M.
Spear G.T.
Abstract: Bacterial vaginosis (BV) is associated with preterm labor, pelvic inflammatory disease (PID) and increased HIV acquisition, although the pathways that mediate these pathological effects have not been elucidated. To determine the presence of Toll-like receptor (TLR)-ligands and their specificity in BV, genital tract fluids were collected from women with and without BV by cervicovaginal lavage (CVL). The CVL samples were evaluated for their ability to stimulate secretion of proinflammatory cytokines and to activate NFκB and the HIV long terminal repeat (LTR), indicators of TLR activation, in human monocytic cells. Stimulation with BV CVLs induced higher levels of IL-8 and TNFα secretion, as well as higher levels of HIV LTR and NFκB activation, than CVLs from women with normal healthy bacterial flora. To identify which TLRs were important in BV, 293 cells expressing specific TLRs were exposed to CVL samples. BV CVLs induced higher IL-8 secretion by cells expressing TLR2 than CVLs from women without BV. Surprisingly, BV CVLs did not stimulate cells expressing TLR4/MD2, although these cells responded to purified lipopolysaccharide (LPS), a TLR4 ligand. BV CVLs, in cells expressing TLR2, also activated the HIV LTR. Thus, these studies show that soluble factor(s) present in the lower genital tract of women with BV activate cells via TLR2, identifying a pathway through which BV may mediate adverse effects. © 2007 Elsevier Ireland Ltd. All rights reserved.
Editor: 
Rights: fechado
Identifier DOI: 10.1016/j.jri.2007.04.004
Address: http://www.scopus.com/inward/record.url?eid=2-s2.0-38149073388&partnerID=40&md5=af78743e490e5c2e925da426258bc003
Date Issue: 2008
Appears in Collections:Unicamp - Artigos e Outros Documentos

Files in This Item:
File SizeFormat 
2-s2.0-38149073388.pdf379.51 kBAdobe PDFView/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.