INIGEM   23989
INSTITUTO DE INMUNOLOGIA, GENETICA Y METABOLISMO
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
B cells in osteoarticular disease caused by Brucella abortus.
Autor/es:
AYELÉN IVANA PESCE VIGLIETTI; PAULA CONSTANZA ARRIOLA BENITEZ; GUILLERMO HERNÁN GIAMBARTOLOMEI; MARIA VICTORIA DELPINO
Reunión:
Congreso; 57. LXIII Reunión Anual de la Sociedad Argentina de Inmunología (SAI). 18-21 Noviembre de 2015.; 2015
Resumen:
B cells in osteoarticular disease caused by Brucella abortus Ayelén Ivana Pesce Viglietti,Paula Constanza Arriola Benitez, Guillermo Hernán Giambartolomei, MariaVictoria Delpino Instituto de Inmunología,Genética y Metabolismo (INIGEM)-CONICET-UBA  Abstract: Osteoarticular brucellosis is the most common localization ofhuman active disease. B cells play an important rol in osteoarticular diseasesince they can produce factors that induce osteoclast differentiation (cellsinvolved in bone resorption). The aim of this study was to determine if Brucellaabortus (Ba) infection could activate B cells. B cells were purified by negative selection using magnetic beads, and depurity was corroborated using anti-CD19-FITC and anti-B220-PE antibodies. Bainfection induces the surface expression of RANKL (p<0.1) (the mainregulator of osteoclastogenesis) and the secretion of MMP-9, TNF-α (p<0.01) and IL6 (p<0.001) by LB. Thesephenomena did not depend on bacterial viability, since they were also inducedby heat-killed Ba (HKBA) (p<0.01). Since osteocytes are the most abundantcells in the bone, and macrophages are the main replication niche for Ba, wedecided to determine if supernatants from Ba-infected osteocytes (MLO-Y4 cellline) and macrophages (J744.A1 cell line) could induce RANKL surface expressionby B cells. Our results indicated that Ba-infected culture supernatants fromosteocytes and macrophages were unable to induce RANKL expression by B cells.Taken together these results indicate that B cells could play a rol inosteoarticular damage during Ba infection through the induction ofosteoclastogenesis by the secretion of proinflamatory cytokines and RANKL.