Platelets Promote Brucella abortus Monocyte Invasion by Establishing Complexes With Monocytes

TROTTA, ALDANA; VELÁSQUEZ, LIS N. (SEGUNDA AUTORA); MILILLO, M. AYELÉN (SEGUNDA AUTORA); DELPINO, M. VICTORIA; RODRÍGUEZ, ANA M.; LANDONI, VERÓNICA I.; GIAMBARTOLOMEI, GUILLERMO H.; POZNER, ROBERTO G.; BARRIONUEVO, PAULA; *AMBAS AUTORAS CONTRIBUYERON DE MANERA EQUIVALENTE AL TRABAJO

Frontiers in Immunology

Frontiers Media SA

Año: 2018 vol. 9

Brucellosis is an infectious disease elicited by bacteria of the genus Brucella. Plateletshave been extensively described as mediators of hemostasis and responsible formaintaining vascular integrity. Nevertheless, they have been recently involved in themodulation of innate and adaptive immune responses. Although many interactions havebeen described between Brucella abortus and monocytes/macrophages, the role ofplatelets during monocyte/macrophage infection by these bacteria remained unknown.The aim of this study was to investigate the role of platelets in the immune responseagainst B. abortus. We first focused on the possible interactions between B. abortus andplatelets. Bacteria were able to directly interact with platelets. Moreover, this interactiontriggered platelet activation, measured as fibrinogen binding and P-selectin expression.We further investigated whether platelets were involved in Brucella-mediated monocyte/macrophage early infection. The presence of platelets promoted the invasion of monocytes/macrophages by B. abortus. Moreover, platelets established complexes withinfected monocytes/macrophages as a result of a carrier function elicited by platelets.We also evaluated the ability of platelets to modulate functional aspects of monocytesin the context of the infection. The presence of platelets during monocyte infectionenhanced IL-1β, TNF-α, IL-8, and MCP-1 secretion while it inhibited the secretion ofIL-10. At the same time, platelets increased the expression of CD54 (ICAM-1) and CD40.Furthermore, we showed that soluble factors released by B. abortus-activated platelets,such as soluble CD40L, platelet factor 4, platelet-activating factor, and thromboxane A2,were involved in CD54 induction. Overall, our results indicate that platelets can directlysense and react to B. abortus presence and modulate B. abortus-mediated infectionof monocytes/macrophages increasing their pro-inflammatory capacity, which couldpromote the resolution of the infection.