Lack of effect of the Salmonella deubiquitinase SseL on the NF-?B pathway.

ABSTRACT: Intracellular replication of Salmonella enterica requires effector proteins translocated across the Salmonella-containing vacuolar membrane by Salmonella pathogenicity island-2 (SPI-2) encoded type III secretion system (T3SS). The SPI-2 T3SS effector SseL is a deubiquitinase that contributes to virulence in mice. Previous work has produced conflicting evidence as to the involvement of SseL in interference with the NF-?B pathway. To attempt to clarify these discrepancies, we compared mRNA levels in mouse primary bone marrow-derived macrophages infected with wild-type or sseL mutant strains using a genome-wide microarray. There was no detectable effect of loss of SseL on mRNA levels corresponding to any known NF-?B-regulated gene. In addition, there was no effect of SseL on (i) the activation or levels of both the canonical inhibitor of the NF-?B pathway (I?B? and phospho-I?B?), and the non-canonical NF-?B precursor p100/p52, (ii) the translocation of the NF-?B transcription factor p65 to the nucleus of infected macrophages and (iii) pro-inflammatory cytokines secretion. Furthermore, ectopic expression of SseL did not affect NF-?B activation in reporter cell lines. These results fail to support a role for SseL in the down-regulation of the host immune response and in particular the NF-?B pathway.

SUBMITTER: Mesquita FS 

PROVIDER: S-EPMC3540083 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature