White MR, Crouch E, Vesona J, Tacken PJ, Batenburg JJ, Leth-Larsen R, Holmskov U, Hartshorn KL. Respiratory Innate Immune Proteins Differentially Modulate the Neutrophil Respiratory Burst Response to Influenza A Virus. Am J Physiol Lung Cell Mol Physiol. 2005 Jun 10; [Epub ahead of print]
Respiratory Innate Immune Proteins Differentially Modulate the Neutrophil Respiratory Burst Response to Influenza A Virus.
White MR, Crouch E, Vesona J, Tacken PJ, Batenburg JJ, Leth-Larsen R, Holmskov U, Hartshorn KL.
Department of Medicine, Boston University School of Medicine, Boston, MA, USA.
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.
White MR, Crouch E, Vesona J, Tacken PJ, Batenburg JJ, Leth-Larsen R, Holmskov U, Hartshorn KL.
Department of Medicine, Boston University School of Medicine, Boston, MA, USA.
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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