Activation of neutrophils by opsonized bacteria (S aureus or E coli, at left) causes the release of bacterially induced microvesicles (b-MV; ∼ 500 nm in diameter). After their release, b-MV can aggregate both nonopsonized and opsonized bacteria, leading to reduced bacterial growth. Released b-MV contain antibacterial proteins myeloperoxidase (MPO) and lactoferrin, and express integrins CD11b and CD18 on their surfaces. Integrins are required for b-MV–mediated bacterial aggregation. This is proposed to be a novel bacteriostatic mechanism for host defense against pathogenic bacteria. Indeed, aggregates of b-MV and bacteria can be detected in the sera of bacteremic patients. Professional illustration by Alice Y. Chen.

Activation of neutrophils by opsonized bacteria (S aureus or E coli, at left) causes the release of bacterially induced microvesicles (b-MV; ∼ 500 nm in diameter). After their release, b-MV can aggregate both nonopsonized and opsonized bacteria, leading to reduced bacterial growth. Released b-MV contain antibacterial proteins myeloperoxidase (MPO) and lactoferrin, and express integrins CD11b and CD18 on their surfaces. Integrins are required for b-MV–mediated bacterial aggregation. This is proposed to be a novel bacteriostatic mechanism for host defense against pathogenic bacteria. Indeed, aggregates of b-MV and bacteria can be detected in the sera of bacteremic patients. Professional illustration by Alice Y. Chen.

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