Brucella abortus ‐infected platelets modulate activation of neutrophils

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

IMMUNOLOGY AND CELL BIOLOGY

NATURE PUBLISHING GROUP

Lugar: Londres; Año: 2020

0818-9641

Brucellosis 5 is a contagious disease caused by bacteria of the genus Brucella.Platelets (PLTs) have been widely involved in the modulation of the immuneresponse. We have previously reported the modulation of Brucella abortus?mediated infection of monocytes. As a result, PLTs cooperate with monocytesand increase their inflammatory capacity, promoting the resolution of theinfection. Extending these results, in this study we demonstrate that patientswith brucellosis present slightly elevated levels of complexes between PLTs andboth monocytes and neutrophils. We then assessed whether PLTs are capableof modulating functional aspects of neutrophils. The presence of PLTsthroughout neutrophils infection increased the production of interleukin-8,CD11b surface expression and reactive oxygen species formation, whereas itdecreased 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 withsupernatants collected from B. abortus?infected PLTs. Our results show thatCD11b expression was induced by PLT?s soluble factors but direct contactbetween cell populations was needed to enhance the respiratory burst.Alternatively, B. abortus?infected PLTs recruit polymorphonuclear (PMN) cellsto the site of infection. Finally, the presence of PLTs did not modify the initialinvasion of PMN cells by B. abortus but improved the restraint of the infectionat extended times. Altogether, our results demonstrate that PLTs interact withneutrophils and promote a proinflammatory phenotype which could alsocontribute to the restraint of the infection.