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1 Department of Medicine, Boston University School of Medicine, Boston, MA, USA
2 Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, USA
3 Department of Biochemistry and Cell Biology, Utrecht University Faculty of Veterinary Medicine, Utrecht, The Netherlands
4 Department of Immunology and Microbiology, University of Southern Denmark, Odense, El Salvador
* To whom correspondence should be addressed. E-mail: khartsho{at}bu.edu.
Oxidants and neutrophils contribute to lung injury during influenza A virus (IAV) infection. Surfactant protein 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, pre-incubation of IAV with SP-D in vitro strongly increases neutrophil respiratory burst responses to the virus. Several factors are shown to modify this apparent pro-inflammatory effect of SP-D. Although multimeric forms of SP-D show dose-dependent augmentation of respiratory burst responses, trimeric, single-arm forms show either no effect or inhibit these responses. Furthermore, if neutrophils are pre-incubated with multimeric SP-D before adding IAV, 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 gp-340 or mucin) significantly reduce the ability of SP-D to promote neutrophil oxidant response. As a result, the net effect of bronchoalveolar lavage (BAL) fluids is to increase neutrophil uptake of IAV while reducing the respiratory burst response to virus.
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