actively inhibits the production of extracellular vesicles by human neutrophils.

is the etiologic agent of the plague. A hallmark of plague is subversion of the host immune response by disrupting host signaling pathways required for inflammation. This non-inflammatory environment permits bacterial colonization and has been shown to be essential for disease manifestation. Previous work has shown that inhibits phagocytosis and degranulation by neutrophils. Manipulation of these key vesicular trafficking pathways suggests that influences EV secretion, cargo selection, trafficking, and/or maturation. Our goal was to define the EV population produced by neutrophils in response to and determine how these vesicles might influence inflammation. Toward these goals, EVs were isolated from human neutrophils infected with or a mutant lacking bacterial effector proteins known to manipulate host cell signaling. Mass spectrometry data revealed that cargoes packaged in EVs isolated from mutant infected cells were enriched with antimicrobials and cytotoxic proteins, contents which differed from uninfected and infected cells. Further, EVs produced in response to lacked inflammatory properties observed in those isolated from neutrophils responding to the mutant. Together, these data demonstrate that actively inhibits the production of antimicrobial EVs produced by neutrophils, likely contributing to immune evasion.