INIGEM   23989
INSTITUTO DE INMUNOLOGIA, GENETICA Y METABOLISMO
Unidad Ejecutora - UE
artículos
Título:
Brucella and osteoarticular cell activation: partners in crime.
Autor/es:
GIAMBARTOLOMEI GUILLERMO H.; ARRIOLA BENITEZ PAULA C.; DELPINO M. VICTORIA; GIAMBARTOLOMEI GUILLERMO H.; ARRIOLA BENITEZ PAULA C.; DELPINO M. VICTORIA
Revista:
Frontiers in Microbiology
Editorial:
Frontiers
Referencias:
Año: 2017
Resumen:
Osteoarticular brucellosis is themost common presentation of human active disease although its prevalence varies widely.The three most common formsof osteoarticular involvement are sacroiliitis, spondylitis, and peripheralarthritis. The molecular mechanisms implicated in bone damage have been recentlyelucidated. B. abortus induces bonedamage through diverse mechanisms in which TNF-α and the receptoractivator of nuclear factor kappa-B ligand (RANKL)-the natural modulator of bone homeostasis  are involved. These processes are driven byinflammatory cells, like monocytes/macrophages, neutrophils, Th17 CD4+T, and B cells. In addition, B. abortushas a direct effect on osteoarticular cells and tilts homeostatic boneremodeling. These bacteria inhibit bone matrix deposition by osteoblasts (theonly bone cells involved in bone deposition), and modify the phenotype of thesecells to produce matrix metalloproteinases (MMPs) and cytokine secretion, contributingto bone matrix degradation. B. abortusalso affects osteoclasts (cells naturally involved in bone resorption) byinducing an increase in osteoclastogenesis and osteoclast activation; thus increasingmineral and organic bone matrix resorption, contributing to bone damage. Giventhat the pathology induced by Brucellaspecies involved joint tissue, experiments conducted on synoviocytes revealedthat besides inducing the activation of these cells to secrete chemokines,proinflammatory cytokines and MMPS, the infection also inhibits synoviocyteapoptosis. Brucella is anintracellular bacterium that replicates preferentially in the endoplasmic reticulum of macrophages. The analysis ofB. abortus-infected synoviocytesindicated that bacteria also replicate in their reticulum suggesting that theycould use this cell type for intracellular replication during theosteoarticular localization of the disease. Finally, the molecular mechanismsof osteoarticular brucellosis discovered recently shed light on how the interactionbetween B. abortus and immune andosteoarticular cells may play an important role in producing damage in jointand bone.