Abstract
Central nervous system (CNS) infections remain a major burden of pediatric disease associated with significant long-term morbidity due to injury to the developing brain. Children are susceptible to various etiologies of CNS infection partly because of vulnerabilities in their peripheral immune system. Young children are known to have reduced numbers and functionality of innate and adaptive immune cells, poorer production of immune mediators, impaired responses to inflammatory stimuli and depressed antibody activity in comparison to adults. This has implications not only for their response to pathogen invasion, but also for the development of appropriate vaccines and vaccination strategies. Further, pediatric immune characteristics evolve across the span of childhood into adolescence as their broader physiological and hormonal landscape develop. In addition to intrinsic vulnerabilities, children are subject to external factors that impact their susceptibility to infections, including maternal immunity and exposure, and nutrition. In this review we summarize the current evidence for immune characteristics across childhood that render children at risk for CNS infection and introduce the link with the CNS through the modulatory role that the brain has on the immune response. This manuscript lays the foundation from which we explore the specifics of infection and inflammation within the CNS and the consequences to the maturing brain in part two of this review series.
Highlights
Central nervous system (CNS) infections in children continue to be an important cause of significant morbidity and mortality, with a predominance in low- and middle-income countries [1,2,3]
We summarize the current evidence for peripheral immune characteristics across childhood that render children at risk for CNS infection and introduce the bidirectional link with the CNS through the modulatory role that the brain has on the immune response
For the purpose of this review we have established the age categories as follows: neonate, infants (0–1 years), preschool children (1–6 years), primary school children (6–12 years), adolescents (12–18 years) and adults (>18 years); unless otherwise stated as specific to the study referenced. This manuscript lays the foundation from which we explore the specifics of infection and inflammation within the CNS and the consequences to the maturing brain in part two of this review series
Summary
Central nervous system (CNS) infections in children continue to be an important cause of significant morbidity and mortality, with a predominance in low- and middle-income countries [1,2,3]. Neonatal monocytes fail to activate adaptive immune cells, either through reduced human leukocyte antigen (HLA)-DR expression or inadequate cytokine production [48]. Schuller et al observed that pDCs of preterm neonates displayed altered morphology and cell function, with significant decreases in the production of IFN-α/β in response to different viral infections [54].
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