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. Author manuscript; available in PMC: 2018 Nov 1.
Published in final edited form as: Trends Microbiol. 2017 Jun 17;25(11):919–931. doi: 10.1016/j.tim.2017.05.013

Figure 2. GBS Interaction with Innate Immune Cells During Genital Infection.

Figure 2

Upon primary vaginal colonization, vaginal-resident mast cells are activated and de-granulated through the hemolytic activity of the GBS pigment. De-granulation leads to the release of inflammatory mediators, including IL-6, IL-8, TNFα, and histamine, which in turn recruits other immune cells, such as neutrophils and macrophages, to aid in bacterial clearance [69]. Neutrophils clear GBS through phagocytosis and extrusion of NETs [67]. Additionally, GBS activates the NLRP3 inflammasome in neutrophils, leading to secretion of IL-1β, as well as other inflammatory cytokines. GBS are able to use the pigment to prevent phagocytic death through sequestration of reactive oxygen species [66], and to avoid being killed by NETs [39]. Macrophages also aid in GBS clearance through phagocytosis. GBS, in turn, activate the NLRP3 inflammasome in macrophages through membrane permeabilization by pigment, leading to pyroptosis and fetal damage during pregnancy [46].