Systemic inflammation is associated with increased risk for prevalent and costly diseases, and animal models implicate the autonomic nervous system in the control of inflammatory processes. In humans, research on autonomic-immune connections has been much more limited, and has focused on single branch autonomic measures (i.e., either parasympathetic or sympathetic). The current study utilized cardiac autonomic balance (CAB), derived from dual-branch cardiac autonomic recordings, to test the relation between resting autonomic function and inflammatory reactivity to challenge in children.

Methods: Participants included 96 children (51 boys, 45 girls) ages 9-11 years (mean age = 9.93 years, SD = 0.57 years). CAB values were calculated from standardized measures of parasympathetic and sympathetic activity, namely resting respiratory sinus arrhythmia and pre-ejection period data, respectively. Children provided two blood samples, one before and one following exposure to an acute social stressor or control condition. Serum was assayed for four cytokines that orchestrate inflammation: interleukin-6 (IL6), interleukin-8 (IL8), interleukin-10 (IL10), and tumor necrosis factor-alpha (TNFa).

Results: We discovered large individual differences in inflammatory marker production across children, and no average main effect of stress condition. CAB significantly predicted these individual differences, such that children lower on CAB showed increasing serum cytokines from time 1 to time 2. In contrast, children with greater CAB tended to show declining inflammatory markers across the session.

Discussion: Low cardiac autonomic balance (i.e., the combination of low parasympathetic and high sympathetic activity) may be a useful marker of proinflammatory tendencies in children, suggesting novel paths for early risk detection and intervention.