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dc.creatorChacón Díaz, Carlos
dc.creatorAltamirano Silva, Pamela
dc.creatorGonzález Espinoza, Gabriela
dc.creatorMedina, María Concepción
dc.creatorAlfaro Alarcón, Alejandro
dc.creatorBouza Mora, Laura
dc.creatorJiménez Rojas, César
dc.creatorWong Araya, Melissa
dc.creatorBarquero Calvo, Elías
dc.creatorRojas Campos, Norman
dc.creatorGuzmán Verri, Caterina
dc.creatorMoreno Robles, Edgardo
dc.creatorChaves Olarte, Esteban
dc.date.accessioned2019-04-08T16:48:46Z
dc.date.available2019-04-08T16:48:46Z
dc.date.issued2015-11-10
dc.identifier.citationhttps://iai.asm.org/content/83/12/4861
dc.identifier.issn1098-5522
dc.identifier.urihttps://hdl.handle.net/10669/76879
dc.description.abstractCanine brucellosis caused by Brucella canis is a disease of dogs and a zoonotic risk. B. canis harbors most of the virulence determinants defined for the genus, but its pathogenic strategy remains unclear since it has not been demonstrated that this natural rough bacterium is an intracellular pathogen. Studies of B. canis outbreaks in kennel facilities indicated that infected dogs displaying clinical signs did not present hematological alterations. A virulent B. canis strain isolated from those outbreaks readily replicated in different organs of mice for a protracted period. However, the levels of tumor necrosis factor alpha, interleukin-6 (IL-6), and IL-12 in serum were close to background levels. Furthermore, B. canis induced lower levels of gamma interferon, less inflammation of the spleen, and a reduced number of granulomas in the liver in mice than did B. abortus. When the interaction of B. canis with cells was studied ex vivo, two patterns were observed, a predominant scattered cell-associated pattern of nonviable bacteria and an infrequent intracellular replicative pattern of viable bacteria in a perinuclear location. The second pattern, responsible for the increase in intracellular multiplication, was dependent on the type IV secretion system VirB and was seen only if the inoculum used for cell infections was in early exponential phase. Intracellular replicative B. canis followed an intracellular trafficking route undistinguishable from that of B. abortus. Although B. canis induces a lower proinflammatory response and has a stealthier replication cycle, it still displays the pathogenic properties of the genus and the ability to persist in infected organs based on the ability to multiply intracellularly.es_ES
dc.description.sponsorshipUniversidad de Costa Rica/[803-B3-761]UCR/Costa Ricaes_ES
dc.description.sponsorshipUniversidad de Costa Rica/[803-B4-654]UCR/Costa Ricaes_ES
dc.description.sponsorshipUniversidad de Costa Rica/[803-B5-653]UCR/Costa Ricaes_ES
dc.description.sponsorshipConsejo Nacional de Ciencia y Tecnología de Costa Rica/[FV-0004-13]/CONICIT/Costa Ricaes_ES
dc.description.sponsorshipInternational Center for Genomic Engineering and Biotechnology/[CRP/12/007]/ICGEB/Indiaes_ES
dc.language.isoen_USes_ES
dc.sourceInfection and Immunity, vol. 83(12), pp. 4861–4870es_ES
dc.subjectAnine brucellosises_ES
dc.subjectDogses_ES
dc.subject579.33 Bastoncitos y cocos aeróbicos gram-negativoses_ES
dc.titleBrucella canis Is an Intracellular Pathogen That Induces a Lower Proinflammatory Response than Smooth Zoonotic Counterpartses_ES
dc.typeartículo original
dc.identifier.doi10.1128/IAI.00995-15
dc.description.procedenceUCR::Vicerrectoría de Investigación::Unidades de Investigación::Ciencias de la Salud::Centro de Investigación en Enfermedades Tropicales (CIET)es_ES
dc.description.procedenceUCR::Vicerrectoría de Docencia::Salud::Facultad de Microbiologíaes_ES
dc.description.procedenceUCR::Vicerrectoría de Investigación::Unidades de Investigación::Ciencias de la Salud::Instituto Clodomiro Picado (ICP)es_ES
dc.identifier.codproyecto803-B4-654
dc.identifier.codproyecto803-B5-653
dc.identifier.codproyecto803-B3-761


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