Not all Group B

Background: Group B Methods: Human THP-1 macrophages were infected with 12 fully characterized clinical GBS isolates representing multiple serotypes, sequence types, clinical presentations, and neonatal gestational ages. Cytokine and chemokine production was quantified at 3 and 24 hours post-infection using LEGENDplex bead-based immunoassays. Caspase-1 activity was measured by bioluminescence, and expression of inflammatory, immunoregulatory, metabolic, and cell death-associated genes were assessed by RT-qPCR at 4 and 24 hours. Data were analyzed using appropriate statistical tests, and multidimensional responses were integrated using radar plot visualization. Results: Macrophage responses to GBS were highly isolate-specific and varied over time. Serotype Ia and Ib isolates triggered rapid inflammasome-associated activation with early IL-1β and IL-18 release and high caspase-1 activity, consistent with pyroptosis. In contrast, serotype II and especially hypervirulent serotype III isolates showed minimal early inflammasome activation but induced delayed immunoregulatory programs marked by elevated IL-10 and Conclusions: This study shows that GBS pathogenicity is not a uniform species-level trait but reflects isolate-specific abilities to reprogram macrophage immunity. By integrating temporal resolution with strain diversity, it provides a mechanistic framework linking macrophage immune trajectories to preterm birth-associated inflammation and heterogeneous outcomes in neonatal infections.