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

ROSET M. S., IBAÑEZ A. E., SPERA J. M., MINATEL L., DE SOUZA FILHO J. A., OLIVEIRA S. C., GIAMBARTOLOMEI G. H., CASSATARO J., BRIONES G.

PLOS ONE

PUBLIC LIBRARY SCIENCE

Lugar: San Francisco; Año: 2014

1932-6203

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