000060671 001__ 60671
000060671 005__ 20190709135437.0
000060671 0247_ $$2doi$$a10.3389/fcimb.2016.00205
000060671 0248_ $$2sideral$$a98082
000060671 037__ $$aART-2017-98082
000060671 041__ $$aeng
000060671 100__ $$0(orcid)0000-0002-9730-2210$$aArias, M.A.
000060671 245__ $$aToll-like receptors 2 and 4 cooperate in the control of the emerging pathogen Brucella microti
000060671 260__ $$c2017
000060671 5060_ $$aAccess copy available to the general public$$fUnrestricted
000060671 5203_ $$aToll-like receptors (TLRs) recognize pathogen-derived molecules and play a critical role during the host innate and adaptive immune response. Brucella spp. are intracellular gram-negative bacteria including several virulent species, which cause a chronic zoonotic infection in a wide range of mammalian hosts known as brucellosis. A new Brucella species, Brucella microti, was recently isolated from wild rodents and found to be highly pathogenic in mice. Using this species-specific model, it was previously found that CD8+ T cells are required to control this infection. In order to find out the role of TLR-mediated responses in the control of this pathogen, the course of infection of B. microti was analyzed over 3 weeks in wild-type (WT) and TLR knock out (KO) mice including TLR2-/-, TLR4-/-, TLR9-/-, TLR2×4-/- and TLR2×4×9-/-. WT and single TLR2, TLR4 and TLR9 KO mice similarly control infection in liver and spleen. In contrast, bacterial clearance was delayed in TLR2×4-/- and TLR2×4×9-/- mice at 7 and 14 days post-infection. This defect correlated with impaired maturation and pro-inflammatory cytokine production in B. microti-infected dendritic cells from TLR2×4-/- and TLR2×4×9-/- mice. Finally, it was found that Tc cells from TLR2×4-/- and TLR2×4×9-/- mice showed reduced ability to inhibit growth of B. microti in macrophages, suggesting the involvement of TLR2 and 4 in the generation of specific Tc cells. Our findings indicate that TLR2 and TLR4 are required to control B. microti infection in mice and that this effect could be related to its participation in the maturation of dendritic cells and the generation of specific CD8+ Tc cells.
000060671 536__ $$9info:eu-repo/grantAgreement/ES/INIA/RTA2013-00065-C02-01$$9info:eu-repo/grantAgreement/ES/MINECO/SAF2014-54763-C2-1-R
000060671 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/
000060671 590__ $$a3.52$$b2017
000060671 591__ $$aMICROBIOLOGY$$b40 / 125 = 0.32$$c2017$$dQ2$$eT1
000060671 591__ $$aIMMUNOLOGY$$b64 / 155 = 0.413$$c2017$$dQ2$$eT2
000060671 592__ $$a1.703$$b2017
000060671 593__ $$aMedicine (miscellaneous)$$c2017$$dQ1
000060671 593__ $$aInfectious Diseases$$c2017$$dQ1
000060671 593__ $$aMicrobiology (medical)$$c2017$$dQ1
000060671 593__ $$aMicrobiology$$c2017$$dQ1
000060671 593__ $$aImmunology$$c2017$$dQ2
000060671 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000060671 700__ $$0(orcid)0000-0002-1861-5981$$aSantiago, L.$$uUniversidad de Zaragoza
000060671 700__ $$aCostas-Ramon, S.
000060671 700__ $$0(orcid)0000-0002-8731-4269$$aJaime-Sánchez, P.$$uUniversidad de Zaragoza
000060671 700__ $$aFreudenberg, M.
000060671 700__ $$0(orcid)0000-0002-5490-5177$$aJiménez de Bagüés, M.P.
000060671 700__ $$0(orcid)0000-0003-0154-0730$$aPardo, J.$$uUniversidad de Zaragoza
000060671 7102_ $$11008$$2566$$aUniversidad de Zaragoza$$bDpto. Microb.Med.Pr.,Sal.Públ.$$cÁrea Inmunología
000060671 7102_ $$11002$$2060$$aUniversidad de Zaragoza$$bDpto. Bioq.Biolog.Mol. Celular$$cÁrea Bioquímica y Biolog.Mole.
000060671 773__ $$g6 (2017), [9 pp.]$$tFrontiers in cellular and infection microbiology$$x2235-2988
000060671 8564_ $$s1926179$$uhttps://zaguan.unizar.es/record/60671/files/texto_completo.pdf$$yVersión publicada
000060671 8564_ $$s12094$$uhttps://zaguan.unizar.es/record/60671/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000060671 909CO $$ooai:zaguan.unizar.es:60671$$particulos$$pdriver
000060671 951__ $$a2019-07-09-11:34:37
000060671 980__ $$aARTICLE