In young children, pneumococcal meningitis epitomizes the paradigm of a destructive innate inflammatory response in the central nervous system: a five-alarm fire. In contrast, cell-free bacterial components reaching the fetal brain from an infected mother signal a quiet, noninflammatory immune response that drives abnormal neurodevelopment, changing brain architecture through neuroproliferation. This review addresses the difference between prenatal and postnatal bacterial-host signaling within the brain.
Keywords: brain; fetus; meningitis; neurodevelopment; pneumococcus.
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