The presence of GBS and its ability to precisely mimic host sialic acids also influences the severity of urinary tract infection (UTI) caused by E. coli, the most common cause of human UTI.
Figure 1. Isogenic GBS with high and low levels of O-acetylation were subjected to commercial sialidases cloned from several gut pathogens. GBS with higher levels of O-acetylation retained more sialic acid upon sialidase exposure. This data was published in Weiman et al, Glycobiology, 2009.
Figure 2. Experiments with murine polymorphonuclear cells (PMNs) in vitro (LEFT) demonstrate that high levels of sialic acid O-acetylation impair the ability of GBS to 1) evade oxidative burst responses of PMNs, and 2) evade killing by PMNs. In the mouse urinary tract in vivo (RIGHT top), highly O-acetylated GBS are less virulent than their low O-acetylated counterparts (~5-fold difference). This defect in survival in the urinary tract was much more pronounced in competition experiments (see Kline et al, Infect. and Immun, 2011).