Outer membrane vesicle-mediated serum protection in .

belongs to the HACEK group of fastidious Gram-negative organisms, a recognized cause of infective endocarditis. is also implicated in periodontitis, with rapid progress in adolescents. We recently demonstrated that the major outer membrane protein, OmpA1 was critical for serum survival of the serotype a model strain, D7SS, and that the paralogue, OmpA2 could operate as a functional homologue to OmpA1 in mediating serum resistance. In the present work, an essentially serum-sensitive double mutant strain derivative was exploited to elucidate if OMVs can contribute to bacterial serum resistance. Indeed, supplementation of OMVs resulted in a dose-dependent increase of the survival of the serum-sensitive strain in incubations in 50% normal human serum (NHS). Whereas neither OmpA1 nor OmpA2 was required for the OMV-mediated serum protection, OMVs and LPS from an strain lacking the LPS O-antigen polysaccharide part were significantly impaired in protecting D7SS . Our results using a complement system screen assay support a model where OMVs can act as a decoy, which can trigger complement activation in an LPS-dependent manner, and consume complement components to protect serum-susceptible bacterial cells.