Fig. 3: Natural anti-E. coli antibodies selectively protect neonates through opsonization.
From: Natural maternal immunity protects neonates from Escherichia coli sepsis
a, Bacterial burden 1 day after UTI89 infection (200 CFU, intraperitoneal inoculation) in 3-day-old pups administered sera from control mice without EcN colonization (n = 8) compared with sera from EcN-colonized wild-type (n = 5) or EcN-colonized μMT−/− (n = 8) donors. b, Bacterial burden 1 day after UTI89 infection in 3-day-old pup or eight-week-old adult FcγRnull, C3−/−, C1q−/− or Cd22−/− recipients administered sera from EcN-colonized wild-type donor mice (n = 6 to 8 mice per group; each dot represents data from one mouse) compared with sera from control mice without E. coli colonization (n = 6 to 8 mice per group; each dot represents data from one mouse). c, EcN opsonization by sera from control mice without EcN colonization (n = 7) compared with sera from wild-type (n = 7), μMT−/− (n = 7) or C3−/− (n = 7) EcN-colonized donors in RAW264.7 mouse macrophage cells. d, EcN opsonization by sera from control mice without E. coli colonization (n = 6) compared with sera from EcN-colonized donors (n = 6) with anti-CD16 and anti-CD32 Fc blockade (anti-CD16/32) or rat IgG2b isotype control antibody in RAW264.7 mouse macrophage cells. e, Opsonization of E. coli (pooled mix of neonatal clinical isolates RS218, SCB12, SCB29, SCB61, SCB34, SCB58, SCB37 and SCB60) by cord blood sera from term pregnancy after heat inactivation, supplementation with IgG-depleted human sera, or with anti-human Fc block, compared with goat polyclonal IgG isotype control antibody in THP1 activated human macrophage cells (left) or HL60 human differentiated neutrophil cells (right) (n = 8 unique cord blood specimens per group (THP1 cells); n = 6 unique cord blood specimens per group (HL60 cells)). Data are presented as mean ± s.d. Differences between groups were analysed using one-way ANOVA (a,c–e) or unpaired Student’s t-test (b).
