Brucella abortus-infected platelets modulate activation of neutrophils

TROTA ALDANA; MILILLO AYELÉN; SERAFINO AGUSTINA; CASTILLO LUIS; BIRNBERG WEISS FEDERICO; DELPINO M. VICTORIA; GIAMBARTOLOMEI GUILLERMO; FERNANDEZ GABRIELA; BARRIONUEVO PAULA

IMMUNOLOGY AND CELL BIOLOGY

NATURE PUBLISHING GROUP

Lugar: Londres; Año: 2020

0818-9641

Brucellosis is a contagious disease caused by bacteria of the genus Brucella. Platelets have been widely involved in the modulation of the immune response. We have previously reported the modulation of Brucella abortus-mediated infection of monocytes. As a result, platelets cooperate with monocytes and increase their inflammatory capacity, promoting the resolution of the infection. Extending these results, in this study we demonstrate that patients with brucellosis present slightly elevated levels of complexes between platelets and both monocytes and neutrophils. We then assessed whether platelets are capable of modulating functional aspects of neutrophils. The presence of platelets throughout neutrophils infection increased the production of IL-8, CD11b surface expression and ROS formation while decreased the expression of CD62L, indicating an activated status of these cells. We next analyzed whether this modulation was mediated by released factors. To discriminate between these options, neutrophils were treated with supernatants collected from B. abortus-infected platelets. Our results show that CD11b expression was induced by platelet?s soluble factors but direct contact between cell populations was needed to enhance the respiratory burst. Alternatively, B. abortus-infected platelets recruit PMN to the site of infection. Finally, the presence of platelets did not modify the initial invasion of PMN by B. abortus but improved the restraint of the infection at extended times. Altogether, our results demonstrate that platelets interact with neutrophils and promote a pro-inflammatory phenotype which could also contribute to the restraint of the infection.