Aging Promotes Neutrophil-Induced Mortality by Augmenting IL-17 Production during Viral Infection Academic Article uri icon


MeSH Major

  • Aging
  • Herpes Simplex
  • Herpesvirus 2, Human
  • Interleukin-17
  • Lymphocyte Activation
  • Natural Killer T-Cells
  • Neutrophil Activation


  • Morbidity and mortality associated with viral infections increase with age, although the underlying mechanisms are unclear. Here, we investigated whether aging alters inflammatory responses during systemic viral infection and thereby contributes to virus-induced death. We found that infection of aged mice with systemic herpes viruses led to rapid increases in serum IL-17, neutrophil activation, and mortality due to hepatocyte necrosis. In contrast, all young mice survived infection, displaying weaker IL-17 induction and neutrophil activation. Natural killer T (NKT) cells isolated from the livers of aged mice produced more IL-17 than did young cells, and adoptively transferred aged NKT cells induced liver injury in young mice impaired in viral control. Importantly, IL-17 neutralization or neutrophil depletion during viral infection reduced liver damage and prevented death of aged mice. These results demonstrate that, during systemic viral infection, aging alters the host-pathogen interaction to overproduce IL-17, contributing to liver injury and death.

publication date

  • November 19, 2009



  • Academic Article



  • eng

PubMed Central ID

  • PMC2779161

Digital Object Identifier (DOI)

  • 10.1016/j.chom.2009.09.011

PubMed ID

  • 19917499

Additional Document Info

start page

  • 446

end page

  • 56


  • 6


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