Show simple item record

dc.creatorMora Cartín, Ricardo
dc.creatorChacón Díaz, Carlos
dc.creatorGutiérrez Jiménez, Cristina
dc.creatorGurdián Murillo, Stephany
dc.creatorLomonte, Bruno
dc.creatorChaves Olarte, Esteban
dc.creatorBarquero Calvo, Elías
dc.creatorMoreno Robles, Edgardo
dc.date.accessioned2017-07-13T19:49:51Z
dc.date.available2017-07-13T19:49:51Z
dc.date.issued2016-06
dc.identifier.citationhttp://iai.asm.org/content/84/6/1712.full.pdf+htmles_ES
dc.identifier.issn0019-9567
dc.identifier.issn1098-5522
dc.identifier.otherPMC4907143
dc.identifier.urihttps://hdl.handle.net/10669/30356
dc.description.abstractBrucella abortus is an intracellular pathogen of monocytes, macrophages, dendritic cells, and placental trophoblasts. This bacterium causes a chronic disease in bovines and in humans. In these hosts, the bacterium also invades neutrophils; however, it fails to replicate and just resists the killing action of these leukocytes without inducing significant activation or neutrophilia. Moreover, B. abortus causes the premature cell death of human neutrophils. In the murine model, the bacterium is found within macrophages and dendritic cells at early times of infection but seldom in neutrophils. Based on this observation, we explored the interaction of mouse neutrophils with B. abortus. In contrast to human, dog, and bovine neutrophils, naive mouse neutrophils fail to recognize smooth B. abortus bacteria at early stages of infection. Murine normal serum components do not opsonize smooth Brucella strains, and neutrophil phagocytosis is achieved only after the appearance of antibodies. Alternatively, mouse normal serum is capable of opsonizing rough Brucella mutants. Despite this, neutrophils still fail to kill Brucella, and the bacterium induces cell death of murine leukocytes. In addition, mouse serum does not opsonize Yersinia enterocolitica O:9, a bacterium displaying the same surface polysaccharide antigen as smooth B. abortus. Therefore, the lack of murine serum opsonization and absence of murine neutrophil recognition are specific, and the molecules responsible for the Brucella camouflage are N-formyl-perosamine surface homopolysaccharides. Although the mouse is a valuable model for understanding the immunobiology of brucellosis, direct extrapolation from one animal system to another has to be undertaken with caution.es_ES
dc.description.sponsorshipFondo Especial de la Educación Superior/[UNA-SIA-0505-13]/FEES-CONARE/Costa Ricaes_ES
dc.description.sponsorshipFondo Especial de la Educación Superior/[UNA-SIA-0504-13]/FEES-CONARE/Costa Ricaes_ES
dc.description.sponsorshipFondo Especial de la Educación Superior/[UNA-SIA-0248-13]/FEES-CONARE/Costa Ricaes_ES
dc.description.sponsorshipFondo Especial de la Educación Superior/[UNA-SIA-0434-14]/FEES-CONARE/Costa Ricaes_ES
dc.description.sponsorshipConsejo Nacional para Investigaciones Científicas y Tecnológicas/[FV-0004-13]/CONICIT-FORINVES/Costa Ricaes_ES
dc.description.sponsorshipThe International Center for Genomic Engineering and Biotechnology/[CRP/12/007]/ICGEB/Indiaes_ES
dc.description.sponsorshipUniversidad de Costa Rica/[803-B3-761]/UCR/Costa Ricaes_ES
dc.language.isoen_USes_ES
dc.sourceInfection and Immunity; Volume 84, Número 6. 2016es_ES
dc.subjectBrucella abortuses_ES
dc.subjectN-formyl-perosaminees_ES
dc.subjectInfectiones_ES
dc.titleN-Formyl-Perosamine Surface Homopolysaccharides Hinder the Recognition of Brucella abortus by Mouse Neutrophilses_ES
dc.typeartículo científicoes_ES
dc.identifier.doi10.1128/IAI.00137-16
dc.description.procedenceUCR::Vicerrectoría de Investigación::Unidades de Investigación::Ciencias de la Salud::Centro de Investigación en Enfermedades Tropicales (CIET)es_ES
dc.identifier.pmid27001541


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record