Brucella abortus–infected platelets modulate the activation of neutrophils

TROTTA, ALDANA; CASTILLO, LUIS A; GIAMBARTOLOMEI, GUILLERMO H; TROTTA, ALDANA; CASTILLO, LUIS A; GIAMBARTOLOMEI, GUILLERMO H; SERAFINO, AGUSTINA; DELPINO, M VICTORIA; BARRIONUEVO, PAULA; SERAFINO, AGUSTINA; DELPINO, M VICTORIA; BARRIONUEVO, PAULA; MILILLO, M AYELÉN; BIRNBERG WEISS, FEDERICO; FERNÁNDEZ, GABRIELA C; MILILLO, M AYELÉN; BIRNBERG WEISS, FEDERICO; FERNÁNDEZ, GABRIELA C

IMMUNOLOGY AND CELL BIOLOGY

NATURE PUBLISHING GROUP

Año: 2020 vol. 98 p. 743 - 756

0818-9641

Brucellosis is a contagious disease caused by bacteria of the genus Brucella. Platelets (PLTs) 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, PLTs 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 PLTs and both monocytes and neutrophils. We then assessed whether PLTs were capable of modulating functional aspects of neutrophils. The presence of PLTs throughout neutrophil infection increased the production of interleukin-8, CD11b surface expression and reactive oxygen species formation, whereas it 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 PLTs. Our results show that CD11b expression was induced by soluble factors of PLTs but direct contact between cell populations was needed to enhance the respiratory burst. Additionally, B. abortus?infected PLTs recruit polymorphonuclear (PMN) cells to the site of infection. Finally, the presence of PLTs did not modify the initial invasion of PMN cells by B. abortus but improved the control of the infection at extended times. Altogether, our results demonstrate that PLTs interact with neutrophils and promote a proinflammatory phenotype which could also contribute to the resolution of the infection.