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This Article Full Text Full Text (PDF) All Versions of this Article: 289/4/L606    most recent 00130.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (14) Citing Articles via Google Scholar Google Scholar Articles by White, M. R. Articles by Hartshorn, K. L. Search for Related Content PubMed PubMed Citation Articles by White, M. R. Articles by Hartshorn, K. L.

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

¹Department of Medicine, Section of Hematology/Oncology, Boston University School of Medicine, Boston Massachusetts; ²Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri; ³Department of Biochemistry and Cell Biology, Utrecht University Faculty of Veterinary Medicine, Utrecht, Netherlands; and ⁴Department of Immunology and Microbiology, University of Southern Denmark, Odense, Denmark

Submitted 23 March 2005 ; accepted in final form 5 June 2005

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.

surfactant protein D; surfactant protein A; collectin; glycoprotein-340; bispecific protein

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