NOD-like receptor activation by outer membrane vesicles from XXXX non-O1 non-O139 strains is modulated by the quorum-sensing regulator HapR.

@entity1 @entity32 @entity1838 @entity368 @entity294 @entity377 @entity6820 @entity18506
@entity1838 is an inhabitant of aquatic systems and one of the causative agents of severe dehydrating @entity294 in @entity1 . It has also emerged as an important cause of different kinds of @entity32 responses, and in particular, @entity1838 strains of the non-O1 non-O139 serogroups (NOVC) have been associated with such infections in @entity1 . We analyzed the potential of outer membrane vesicles (OMVs) derived from the NOVC strain V:5/04 to induce @entity32 responses in @entity1 host cells. V:5/04 OMVs were taken up by @entity1 epithelial cells and induced @entity32 responses. Small interfering RNA (siRNA)-mediated gene knockdown revealed that the @entity32 potential of NOVC OMVs was partially mediated by the @entity377 -binding domain-, @entity368 -rich repeat-containing family member @entity18506 . Physiochemical analysis of the content of these OMVs, in conjunction with @entity18506 and @entity6820 reporter assays in HEK293T cells, confirmed the presence of both @entity18506 and @entity6820 active peptidoglycan in the OMVs. Furthermore, we show that deletion of the quorum-sensing regulator HapR, which mimics an infective life style, specifically reduced the @entity32 potential of the V:5/04 OMVs and their ability to activate @entity18506 and @entity6820 . In conclusion, our study shows that NOVC OMVs elicit immune responses mediated by @entity18506 and @entity6820 in @entity1 host cells. Moreover, we provide evidence that the quorum-sensing machinery plays an important regulatory role in this process by attenuating the @entity32 potential of OMVs under infective conditions. This work thus identifies a new facet of how Vibrio affects host immune responses and defines a role for the quorum-sensing machinery in this process.
