Respiratory innate immune proteins differentially modulate the neutrophil respiratory burst response to influenza A virus

Mitchell M. White, Erika Crouch, Jenny Vesona, Paul J. Tacken, Joseph J. Batenburg, Rikke Leth-Larsen, Uffe Holmskov, Kevan L. Hartshorn

Research output: Contribution to journalArticlepeer-review

52 Scopus citations

Abstract

Oxidants and neutrophils contribute to lung injury during influenza A virus (IAV) infection. Surfactant protein (SP)-D plays a pivotal role in restricting IAV replication and inflammation in the first several days after infection. Despite its potent anti-inflammatory effects in vivo, preincubation of IAV with SP-D in vitro strongly increases neutrophil respiratory burst responses to the virus. Several factors are shown to modify this apparent proinflammatory effect of SP-D. Although multimeric forms of SP-D show dose-dependent augmentation of respiratory burst responses, trimeric, single-arm forms either show no effect or inhibit these responses. Furthermore, if neutrophils are preincubated with multimeric SP-D before IAV is added, oxidant responses to the virus are significantly reduced. The ability of SP-D to increase neutrophil uptake of IAV can be dissociated from enhancement of oxidant responses. Finally, several other innate immune proteins that bind to SP-D and/or IAV (i.e., SP-A, lung glycoprotein-340 or mucin) significantly reduce the ability of SP-D to promote neutrophil oxidant response. As a result, the net effect of bronchoalveolar lavage fluids is to increase neutrophil uptake of IAV while reducing the respiratory burst response to virus.

Original languageEnglish
Pages (from-to)L606-L616
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume289
Issue number4 33-4
DOIs
StatePublished - Oct 2005

Keywords

  • Bispecific protein
  • Collectin
  • Glycoprotein-340
  • Surfactant protein A
  • Surfactant protein D

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