Cited by 61Neutrophil, Myeloperoxidase and Oxidative MechanismsInflammation biomarkers and pathwaysInfluenza Virus Research Studies

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

White, Mitchell R., Crouch, Erika, Vesona, Jenny, Tacken, Paul J., Batenburg, Joseph J., Leth-Larsen, Rikke, Holmskov, Uffe, Hartshorn, Kevan L.·2005·American Journal of Physiology-Lung Cellular and Molecular Physiology

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.

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Crossref · 10.1152/ajplung.00130.2005

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  • In both scenarios, function of the effector cells is impaired by influenza virus infection, so only the harmful effects of the inflammatory response are realized.

    “In both scenarios, function of the effector cells is impaired by influenza virus infection, so only the harmful effects of the inflammatory response are realized [33,[44][45][46].”

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Authors
White, M. R., Crouch, E., Vesona, J., Tacken, P. J., Batenburg, J. J., Leth-Larsen, R., Holmskov, U., & Hartshorn, K. L.
Affiliations
Boston University (US)
Venue
American Journal of Physiology-Lung Cellular and Molecular Physiology
Published
2005-10
Volume
289
Issue
4
Pages
L606-L616
ISSN
  • 1040-0605 (ISSN-L)
  • 1522-1504
OpenAlex
W2139266182
Cited by
61
References
50
Citations by year
2025: 1 · 2024: 1 · 2023: 3 · 2022: 1 · 2021: 2 · 2020: 2 · 2019: 1 · 2018: 1 · 2017: 5 · 2016: 3 · 2015: 3 · 2014: 1 · 2013: 1 · 2012: 2
FWCI
2.25
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Lung Cellular and Molecular Physiology (publishedVersion)
  • PubMed (publishedVersion)
  • University of Southern Denmark Research Portal (University of Southern Denmark) (publishedVersion)
  • Radboud Repository (Radboud University) (submittedVersion)
Funders
National Heart, Lung, and Blood Institute (P01HL029594, R01HL044015, HL- 44015, HL-69031, HL 29594, R01HL069031)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
  • Health Sciences › Medicine › Epidemiology › Influenza Virus Research Studies
Keywords
influenza A virus, surfactant protein D, neutrophils, respiratory burst, innate immunity, surfactant protein A, mucin, neutrophil phagocytosis, lung injury, bronchoalveolar lavage fluid
MeSH terms
Animals, Bronchoalveolar Lavage Fluid, Chick Embryo, Cricetinae, Humans, Hydrogen Peroxide, Influenza, Human, Lung, Neutrophils, Influenza A virus, Receptors, Immunologic, Recombinant Proteins, CHO Cells, Respiratory Burst, Pulmonary Surfactant-Associated Protein A, Pulmonary Surfactant-Associated Protein D

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