Journal
PEDIATRIC RESEARCH
Volume 80, Issue 5, Pages 702-709Publisher
SPRINGERNATURE
DOI: 10.1038/pr.2016.130
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Funding
- National Institute of Health (Bethesda, MD) [U01 HL102288]
- Children's Miracle Network at the University of Iowa
- Division of Pediatric Critical Care at the University of Iowa
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BACKGROUND: Respiratory syncytial virus (RSV) is the leading cause of bronchiolitis and pneumonia in children under 1 y of age in the USA. The host immune response is believed to contribute to RSV-induced disease. We hypothesize that severe RSV infection in infants is mediated by insufficient regulation of the host immune response of regulatory T cells (Tregs) resulting in immunopathology. METHODS: Blood and nasal aspirates from 23 RSV-infected and 17 control infants under 1 y of age were collected. Treg frequencies were determined by flow cytometry from peripheral blood mononuclear cells. Analysis of 24 cytokines was measured by multiplex assay on nasal aspirates. RESULTS: We demonstrate that the frequency of activated Tregs is significantly reduced in the peripheral blood of RSV-infected infants compared with age-matched controls. Surprisingly, T helper (Th)17 related cytokines including interleukin (IL)-1 beta, IL-17A, and IL-23 were associated with a reduction in clinical symptoms of respiratory distress. In addition, the amount of IL-33 protein in nasal washes, a cytokine important in maintaining Treg homeostasis in mucosal tissues, was decreased in RSV-infected children. CONCLUSION: These results suggest that decreased Treg numbers and an inability to properly control the host inflammatory response results in severe RSV infection.
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