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BackgroundGroup B Streptococcus (GBS) infection causes inflammatory comorbidities in newborns. While the mechanisms remain unclear, evidence suggests that impaired innate-adaptive immune interactions may be contributory. We hypothesized that GBS-stimulated neonatal neutrophils provide a milieu that may drive proinflammatory T-helper (Th) cell programming.MethodsNeutrophils were stimulated with Type III GBS (COH1); supernatants or intact neutrophils were cocultured with CD4 + T cells or regulatory T cells (Tregs). Resulting intracellular cytokines and nuclear transcription factors were determined by multicolor flow cytometry.ResultsGBS-stimulated neutrophils released soluble mediators that induced greater interleukin-17 (IL-17) responses in neonatal vs. adult CD4 + T cells in the absence of added polarizing cytokines. GBS-stimulated neonatal neutrophils also induced robust expression of the canonical nuclear transcription factors for Th1 (Tbet) and Th17 (IL-17) cells in CD4 + T cells. Following GBS stimulation, both intact neutrophils and neutrophil-derived mediators promoted the generation of Tregs with Th1 and Th17 characteristics.ConclusionGBS-stimulated neonatal neutrophils bias the in vitro Th differentiation program of neonatal CD4 + T cells and promote proinflammatory Th1 and Th17 phenotypes in Tregs. Our data suggest that developmental modifications of innate-adaptive immune cross-talk mechanisms may contribute to the inflammatory complications associated with neonatal GBS infection.

Neonatal neutrophils stimulated by group B Streptococcus induce a proinflammatory T-helper cell bias