Brucella abortus ‐infected platelets modulate activation of neutrophils

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

IMMUNOLOGY AND CELL BIOLOGY

NATURE PUBLISHING GROUP

Año: 2020

0818-9641

Brucellosis is a contagious disease caused by bacteria of the genus Brucella. Platelets havebeen widely involved in the modulation of the immune response. We have previouslyreported the modulation of Brucella abortus-mediated infection of monocytes. As a result,platelets cooperate with monocytes and increase their inflammatory capacity, promotingthe resolution of the infection. Extending these results, in this study we demonstrate thatpatients with brucellosis present slightly elevated levels of complexes between plateletsand both monocytes and neutrophils. We then assessed whether platelets are capable ofmodulating functional aspects of neutrophils. The presence of platelets throughoutneutrophils infection increased the production of IL-8, CD11b surface expression and ROSformation while decreased the expression of CD62L, indicating an activated status of thesecells. We next analyzed whether this modulation was mediated by released factors. Todiscriminate between these options, neutrophils were treated with supernatants collectedfrom B. abortus-infected platelets. Our results show that CD11b expression was induced byplatelet?s soluble factors but direct contact between cell populations was needed to enhancethe respiratory burst. Alternatively, B. abortus-infected platelets recruit PMN to the site ofinfection. Finally, the presence of platelets did not modify the initial invasion of PMN byB. abortus but improved the restraint of the infection at extended times. Altogether, ourresults demonstrate that platelets interact with neutrophils and promote a pro-inflammatoryphenotype which could also contribute to the restraint of the infection.