Host-to-Pathogen Transfer of Neutrophil Components via Extracellular Vesicles Shields Candida albicans from Immune Attack in Human Blood

ABSTRACT: Neutrophils effectively eliminate Candida albicans from human blood, but a subset of C. albicans escapes their activity and remains extracellular and viable. Here we show that this is independent from known immune-escape traits of this fungal pathogen. Instead, neutrophil-derived extracellular vesicles (EVs) enriched in antimicrobial proteins and neutrophil surface markers (CD66b, CD11b, CD45, CD63; CR1/3/4 components) promote this state. EVs bind to C. albicans in a complement-dependent manner that required prior C3b/iC3b deposition and was partially blocked by anti-CD11b, consistent with CR3 engagement. Despite their antimicrobial cargo, EVs did not impair fungal growth. Instead, EV coating reduced neutrophil phagocytosis in both purified-cell and whole-blood settings. These findings reveal a dual role for neutrophil EVs at the host-pathogen interface: although enriched for innate effector molecules, their deposition on C. albicans does not impair growth but is associated with reduced phagocytic uptake and maintenance of an extracellular population.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Neutrophil

SUBMITTER: Thomas Krüger  

LAB HEAD: Thomas Krüger

PROVIDER: PXD070460 | Pride | 2026-09-03

REPOSITORIES: Pride