Impact of neutrophils on antiviral activity of human bronchoalveolar lavage fluid.

@article{White2007ImpactON,
  title={Impact of neutrophils on antiviral activity of human bronchoalveolar lavage fluid.},
  author={Mitchell R. White and Tesfaldet Tecle and Erika C. Crouch and Kevan L Hartshorn},
  journal={American journal of physiology. Lung cellular and molecular physiology},
  year={2007},
  volume={293 5},
  pages={
          L1293-9
        }
}
  • M. White, T. Tecle, +1 author K. Hartshorn
  • Published 1 November 2007
  • Biology, Medicine
  • American journal of physiology. Lung cellular and molecular physiology
Surfactant protein D (SP-D) and neutrophils participate in the early innate immune response to influenza A virus (IAV) infection. SP-D increases neutrophil uptake of IAV and modulates neutrophil respiratory burst responses to IAV; however, neutrophil proteases have been shown to degrade SP-D, and human neutrophil peptide defensins bind to SP-D and can cause precipitation of SP-D from bronchoalveolar lavage fluid (BALF). BALF has significant antiviral activity against IAV. We first added… 
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39 Citations
Highly Influential Citations
1
Background Citations
16
Methods Citations
1
Results Citations
4

39 Citations

Citation Type

Citation Type

Pulmonary Surfactant Protein D in First-Line Innate Defence against Influenza A Virus Infections
TLDR
SP-D modulates the inflammatory response and helps to maintain a balance between effective neutralization/killing of IAV, and protection against alveolar damage resulting from IAV-induced excessive inflammatory responses.
Critical Role of IL-17RA in Immunopathology of Influenza Infection
TLDR
Data support targeting IL-17 orIL-17RA in acute lung injury due to acute viral infection and shows significantly reduced levels of oxidized phospholipids, which have previously been shown to be an important mediator in several models of acute Lung injury, including influenza infection and gastric acid aspiration.
Host DNA released by NETosis in neutrophils exposed to seasonal H1N1 and highly pathogenic H5N1 influenza viruses
TLDR
The data is the first to demonstrate that NET formation is abrogated in H5N1 influenza virus infection and might contribute to the severity of H5n1 disease.
Immunopathology of Influenza Infection Critical Role of IL-17 RA in Ross
TLDR
Data support targeting IL-17 orIL-17RA in acute lung injury due to acute viral infection and the role of neutrophils in severe influenza infections has been debated.
Role of surfactant protein A and D (SP-A and SP-D) in human antiviral host defense.
TLDR
The relative importance of antiviral vs anti-inflammatory effects of SP-A and SP-D in viral infections and the potential use of these collectins as therapeutics for viral infections are under investigation.
Histone H4 potentiates neutrophil inflammatory responses to influenza A virus: Down-modulation by H4 binding to C-reactive protein and Surfactant protein D
TLDR
It is shown that histone H4 binds to IAV and aggregates viral particles and markedly potentiates IAV induced neutrophil respiratory burst responses, indicating that complexes formed of histones and IAV are a potent neutrophils activating stimulus.
Critical role of interleukin-17 receptor signaling in the immunopathology of influenza infection
TLDR
Evaluated data suggests that IL-17 signaling may be a key event, and intriguing therapeutic target, in the pathogenesis of acute lung injury.
The Role and Molecular Mechanism of Action of Surfactant Protein D in Innate Host Defense Against Influenza A Virus
TLDR
The mechanism of binding of wild type and mutant forms of SP-D have been determined and these studies could guide investigation of the interactions ofSP-D with other pathogens.
Innate Immunity and Influenza A Virus Pathogenesis: Lessons for COVID-19
  • K. Hartshorn
  • Biology, Medicine
    Frontiers in Cellular and Infection Microbiology
  • 2020
TLDR
The role of soluble innate inhibitors including surfactant protein D and antimicrobial peptides that have a potential dual capacity for down-regulating viral replication and also inhibiting excessive inflammatory responses are evaluated and how these innate host factors could possibly be harnessed to treat IAV infection.
Activation of invariant NKT cells enhances the innate immune response and improves the disease course in influenza A virus infection
TLDR
It is shown that activation of iNKT cells with α‐galactosylceramide during influenza virus infection transiently enhanced early innate immune response without affecting T cell immunity, and reduced early viral titres in lungs of C57BL/6 mice.
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References

SHOWING 1-10 OF 40 REFERENCES
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TLDR
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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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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