Brucella cyclic ?-1,2-glucan plays a critical role in the induction of splenomegaly in mice.

ABSTRACT: Brucella, the etiological agent of animal and human brucellosis, is a bacterium with the capacity to modulate the inflammatory response. Cyclic ?-1,2-glucan (C?G) is a virulence factor key for the pathogenesis of Brucella as it is involved in the intracellular life cycle of the bacteria. Using comparative studies with different C?G mutants of Brucella, cgs (C?G synthase), cgt (C?G transporter) and cgm (C?G modifier), we have identified different roles for this polysaccharide in Brucella. While anionic C?G is required for bacterial growth in low osmolarity conditions, the sole requirement for a successful Brucella interaction with mammalian host is its transport to periplasmic space. Our results uncover a new role for C?G in promoting splenomegaly in mice. We showed that C?G-dependent spleen inflammation is the consequence of massive cell recruitment (monocytes, dendritics cells and neutrophils) due to the induction of pro-inflammatory cytokines such as IL-12 and TNF-? and also that the reduced splenomegaly response observed with the cgs mutant is not the consequence of changes in expression levels of the characterized Brucella PAMPs LPS, flagellin or OMP16/19. Complementation of cgs mutant with purified C?G increased significantly spleen inflammation response suggesting a direct role for this polysaccharide.

SUBMITTER: Roset MS 

PROVIDER: S-EPMC4077732 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature