CROSSTALK BETWEEN PLATELETS, B. ABORTUS AND IMMUNE CELLS

TROTTA, ALDANA; MILILLO, M. AYELÉN; DELPINO, M. VICTORIA; GIAMBARTOLOMEI, GUILLERMO; POZNER, ROBERTO G.; VELASQUEZ, LIS N.; BARRIONUEVO, PAULA

Congreso; LXI REUNIÓN ANUAL DE LA SOCIEDAD ARGENTINA DE INVESTIGACIÓN CLÍNICA (SAIC) LXIV REUNIÓN ANUAL DE LA SOCIEDAD ARGENTINA DE INMUNOLOGÍA (SAI) XLVIII REUNIÓN ANUAL DE LA SOCIEDAD ARGENTINA DE FARMACOLOGÍA EXPERIMENTAL (SAFE); 2016

Brucellosis is an infectious disease elicited by bacteria of the genus Brucella. Platelets have been extensively described as mediators of hemostasis and responsible for maintaining vascular integrity. Nevertheless, they have recently got involved in the modulation of innate and adaptive immune responses. We have already demonstrated a crosstalk between B. abortus and monocytes. However, the role of platelets during monocyte/macrophage infection by these bacteria remains unknown. The aim of this study was to investigate whether platelets are involved in the development of Brucella-mediated infection. To start evaluating this, THP-1 cells (pro-monocytic human cell line) were infected with B. abortus-GFP (100:1) in the presence or absence of platelets for 4 h and the effect of platelets on the infectious capacity of Brucella was analyzed by confocal microscopy. Our results showed that the presence of platelets stimulated the invasion of monocytes by B. abortus. Moreover, we observed that platelets formed complexes solely with infected monocytes. Afterwards, we evaluated the ability of platelets to modulate functional aspects of monocytes during the infection. First, we studied the secretion of immunomodulatory mediators. To address this, THP-1 cells were infected with B. abortus in the presence or absence of platelets for 4 or 24 h. The supernatants from infected cells were collected and quantified by ELISA. Next, we studied the expression of adhesion and co-stimulatory molecules on the monocyte surface by flow cytometry. The presence of platelets during monocytes/macrophages infection stimulated IL-1β, IL-8 and MCP-1 secretion (p