Fig. 4: GAS virulence in the subcutaneous infection model is not impacted by IVIG treatments or EndoS-inactivation.
From: Pathogen-driven degradation of endogenous and therapeutic antibodies during streptococcal infections
a Time-dependent weight measurements of infected mice during the course of infection (n = 5 animals/ time point), Data are presented as mean values +/- SEM. b Volcano plots of changes in plasma proteins between uninfected and infected mice with wildtype bacteria, and (c) between animals infected with wildtype vs EndoS (KO) GAS strain at 36 h p.i. where red spheres indicate significantly changed protein abundances. d The levels of plasma leukocyte counts, bacterial burden in (e), skin, and f, liver across the experiments. IVIG antibody titers against GAS-specific (g) M1, (h), C5A peptidase and (i) surface exclusion protein PRGA, as determined by ELISA. FCγ-receptor activity assay of (j), CD16 (FCγ IIIa) and (k), CD32 (FCγ IIa). Both ELISA and cell assays were done in triplicates in two independent experiments, and statistical significance is denoted with stars and was assessed by two-sided Student’s t-test, p < 0.05. Data are presented as mean values +/- SEM. Source data are provided as a Source Data file.
