TY - JOUR
T1 - Polysaccharides and virulence of Burkholderia pseudomallei
AU - Sarkar-Tyson, Mitali
AU - Thwaite, J.E. E.
AU - Harding, S.V. V.
AU - Smither, S.J. J.
AU - Oyston, P.C.F. C.F.
AU - Atkins, T.P. P.
AU - Titball, R.W. W.
PY - 2007
Y1 - 2007
N2 - Burkholderia pseudomallei is the causative agent of melioidosis, an infectious disease of humans and animals. Gene clusters which encode capsular polysaccharide (type I O-PS) and LPS (type II O-PS), both of which play roles in virulence, have previously been identified. Here, the identification of two further putative clusters, type III O-PS and type IV O-PS, is reported. Mice challenged with type III O-PS or type IV O-PS mutants showed increased mean times to death (7.8 and 11.6 days) compared to those challenged with wild-type S. pseudomallei (3 days). To investigate the possible roles of polysaccharides in protection, mice were immunized with killed cells of wild-type B. pseudomallei or killed cells of B. pseudomallei with mutations in the O antigen, capsular polysaccharide, type III O-PS or type IV O-PS gene clusters. Immunization with all polysaccharide mutant strains resulted in delayed time to death compared to the naive controls, following challenge with wild-type S. pseudomallei strain K96243. However, immunization with killed polysaccharide mutant strains conferred different degrees of protection, demonstrating the immunological importance of the polysaccharide clusters on the surface of B. pseudomallei. © 2007 Crown copyright.
AB - Burkholderia pseudomallei is the causative agent of melioidosis, an infectious disease of humans and animals. Gene clusters which encode capsular polysaccharide (type I O-PS) and LPS (type II O-PS), both of which play roles in virulence, have previously been identified. Here, the identification of two further putative clusters, type III O-PS and type IV O-PS, is reported. Mice challenged with type III O-PS or type IV O-PS mutants showed increased mean times to death (7.8 and 11.6 days) compared to those challenged with wild-type S. pseudomallei (3 days). To investigate the possible roles of polysaccharides in protection, mice were immunized with killed cells of wild-type B. pseudomallei or killed cells of B. pseudomallei with mutations in the O antigen, capsular polysaccharide, type III O-PS or type IV O-PS gene clusters. Immunization with all polysaccharide mutant strains resulted in delayed time to death compared to the naive controls, following challenge with wild-type S. pseudomallei strain K96243. However, immunization with killed polysaccharide mutant strains conferred different degrees of protection, demonstrating the immunological importance of the polysaccharide clusters on the surface of B. pseudomallei. © 2007 Crown copyright.
U2 - 10.1099/jmm.0.47043-0
DO - 10.1099/jmm.0.47043-0
M3 - Article
SN - 0022-2615
VL - 56
SP - 1005
EP - 1010
JO - Journal of Medical Microbiology
JF - Journal of Medical Microbiology
IS - 8
ER -