Respiratory Syncytial Virus Disease Is Mediated by Age-Variable IL-33

• DOI: 10.1371/journal.ppat.1005217
• Publication Date: 2015-10-16T18:22:08Z
• Authors: Jordy Saravia; Dahui You; Bishwas Shrestha; Sridhar Jaligama; David Siefker; Greg I. Lee; Jeffrey N. Harding; Tamekia L. Jones; Cynthia Rovnaghi; Bindiya Bagga; John P. DeVincenzo; Stephania A. Cormier
• Keywords: Convalescence

Respiratory syncytial virus (RSV) is the most common cause of infant hospitalizations and severe RSV infections are a significant risk factor for childhood asthma. The pathogenic mechanisms responsible induced immunopathophysiology remain elusive. Using an age-appropriate mouse model RSV, we show that IL-33 plays critical role in immunopathogenesis which associated with higher group 2 innate lymphoid cells (ILC2s) specifically neonates. Infection rapid expression increase ILC2 numbers lungs neonatal mice; this was not observed adult mice. Blocking antibodies or using receptor knockout during infection sufficient to inhibit (i.e., airway hyperresponsiveness, Th2 inflammation, eosinophilia, mucus hyperproduction); whereas administration mice induce disease. Additionally, elevated IL-13 were nasal aspirates from infants hospitalized RSV; these cytokines declined convalescence. In summary, necessary, either directly indirectly, ILC2s biased following infection. This study provides mechanism involving mediated human