The immune-endocrine alterations in osteocytes during Ba infection.

PAULA CONSTANZA ARRIOLA BENITEZ; MARÍA VICTORIA DELPINO; AYELÉN IVANA PESCE VIGLIETTI; ANDREA MOLLI; MARÍA VIRGINIA GENTILINI; GUILLERMO HERNÁN GIAMBARTOLOMEI

Buenos Aires

Congreso; REUNIÓN CONJUNTA DE SOCIEDADES DE BIOCIENCIAS; 2017

Patients with brucellosis have an imbalance in cortisol / DHEA ratio in plasma. Bone remodeling process is regulated by hormones. Then, we aim to study the effect of cortisol and DHEA on osteocytes (the most abundant cells of bone) during B. abortus (Ba) infection. Cortisol treatment inhibited the expression of TNF-α and IL-6 and RANKL (the main regulator of osteoclastogenesis) induced by Ba infection in osteocytes. DHEA reverses the effect of cortisol on TNF-α and RANKL expression, but not on IL-6 expression. Ba infection induce MMP-2 by osteocytes (zymography). When cortisol was added during Ba infection the secretion of MMP-2 was inhibited. When the infection experiments were performed in the presence of both cortisol and DHEA, DHEA could reverse the effect of cortisol on MMP-2 production.RANKL and TNF-α are the main cytokines involved in osteoclastogenesis in inflammatory conditions. We performed osteoclastogenesis experiments by added supernatants from osteocytes infected with Ba in the presence of cortisol and DHEA to precursors (RAW 264.7) in the presence of M-CSF. Our results indicated that cortisol inhibit the osteoclastogenesis induced by supernatants from Ba infected osteocytes. It is known that cortisol regulates target genes by binding to the glucocorticoid receptor (GR). Ba infection inhibited GR-α and GR-β expression (p