Chicken dendritic cells are susceptible to highly pathogenic avian influenza viruses which induce strong cytokine responses

Dev Comp Immunol. 2013 Mar;39(3):198-206. doi: 10.1016/j.dci.2012.10.011. Epub 2012 Nov 23.

Abstract

Infection with highly pathogenic avian influenza (HPAI) in birds and mammals is associated with severe pathology and increased mortality. We hypothesize that in contrast to low pathogenicity avian influenza (LPAI) infection, HPAI infection of chicken dendritic cells (DC) induces a cytokine deregulation which may contribute to their highly pathogenic nature. Infection of DC with LPAI H7N1 and H5N2 resulted in viral RNA and NP expression without increase in time, in contrast to HPAI H7N1 and H5N2 mRNA expression. No increase in IFN mRNA was detected after infection with LPAI, but after LPAI H5N2, and not LPAI H7N1, infection the level of bioactive IFNα/β significantly increased. After HPAI H7N1 and H5N2 infection, significant increases in IL-8, IFN-α, IFN-γ mRNA expression and in TLR1, 3, and 21 mRNA were observed. This enhanced activation of DC after HPAI infection may trigger deregulation of the immune response as seen during HPAI infection in chickens.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cells, Cultured
  • Chickens / immunology*
  • Chickens / virology
  • Cytokines / genetics
  • Cytokines / metabolism
  • Dendritic Cells / immunology*
  • Dendritic Cells / virology
  • Disease Susceptibility
  • Immunity, Cellular
  • Influenza A Virus, H5N2 Subtype / immunology*
  • Influenza A Virus, H5N2 Subtype / pathogenicity
  • Influenza A Virus, H5N2 Subtype / physiology*
  • Influenza A Virus, H7N1 Subtype / pathogenicity
  • Influenza A Virus, H7N1 Subtype / physiology*
  • Influenza in Birds / immunology*
  • Influenza in Birds / physiopathology
  • Species Specificity
  • Toll-Like Receptor 1 / genetics
  • Toll-Like Receptor 1 / metabolism
  • Toll-Like Receptor 3 / genetics
  • Toll-Like Receptor 3 / metabolism
  • Up-Regulation
  • Virus Replication

Substances

  • Cytokines
  • Toll-Like Receptor 1
  • Toll-Like Receptor 3