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Cutting Edge: Sympathetic Nervous System Increases Proinflammatory Cytokines and Exacerbates Influenza A Virus Pathogenesis

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Grebe, Kristie M, Takeda, Kazuyo, Hickman, Heather D, Bailey, Adam M, Embry, Alan C, Bennink, Jack R, Yewdell, Jonathan W·2010·The Journal of Immunology
DOI 10.4049/jimmunol.0903395PMC PMC2941093
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Abstract

Although the sympathetic nervous system innervates the lung, little is known about its participation in host immunity to pulmonary pathogens. In this study, we show that peripheral sympathectomy reduces mouse morbidity and mortality from influenza A virus-induced pneumonia due to reduced inflammatory influx of monocytes, neutrophils, and NK cells. Mortality was also delayed by treating mice with an α-adrenergic antagonist. Sympathectomy diminished the immediate innate cytokine responses, particularly IL-1, which was profoundly reduced. These findings demonstrate an unexpected role for the sympathetic nervous system in innate antiviral immunity and in exacerbating the pathology of a virus of great significance to human and animal health.

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  • SNS activation enhances transcription of proinflammatory immune response genes, increasing systemic inflammatory activity that aids in combating bacteria and other extracellular pathogens.

    “SNS activation enhances transcription of proinflammatory immune response genes (S. W. Cole et al., 2010; Grebe et al., 2010), which increases systemic inflammatory activity that aids in combating bacteria and other extracellular pathogens”

    From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Grebe et al., 2010

    The Abstract (page unavailable) reports that removing peripheral SNS input diminished innate cytokine responses and inflammatory-cell influx in mice with influenza A pneumonia. The Results and Discussion also link SNS activity to IL-1 and IL-6 secretion. The paper does not establish enhanced gene transcription, a systemic inflammatory effect, or protection against bacteria and other extracellular pathogens; its reported inflammatory effect worsened influenza pathology. (LLM, conf=0.86)

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Research works printed but not linked: 20

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Authors
Grebe, K. M., Takeda, K., Hickman, H. D., Bailey, A. M., Embry, A. C., Bennink, J. R., & Yewdell, J. W.
Affiliations
National Institutes of Health (US)
Corresponding author
Yewdell, Jonathan W
ORCID
Venue
The Journal of Immunology
Publisher
Oxford University Press (OUP)
Published
2009-12-27
Volume
184
Issue
2
Pages
540-544
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
DOI
10.4049/jimmunol.0903395
PMC
PMC2941093
OpenAlex
W2158175641
Cited by
130
References
0
Citations by year
2026: 5 · 2025: 8 · 2024: 8 · 2023: 8 · 2022: 6 · 2021: 13 · 2020: 13 · 2019: 9 · 2018: 5 · 2017: 5 · 2016: 11 · 2015: 8 · 2014: 11 · 2013: 6 · 2012: 5
FWCI
3.15
Type
journal article
Language
en
Open access
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations
  • The Journal of Immunology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Institute of Allergy and Infectious Diseases (Z01AI001054)
Topics
  • Health Sciences › Medicine › Epidemiology › Influenza Virus Research Studies
  • Life Sciences › Neuroscience › Neurology › Vagus Nerve Stimulation Research
  • Health Sciences › Medicine › Psychiatry and Mental health › Cancer, Stress, Anesthesia, and Immune Response
Keywords
sympathetic nervous system, influenza A virus, viral pneumonia, inflammatory cytokines, innate immunity, sympathectomy, alpha-blockers, interleukin-1, monocytes, neutrophils, natural killer cells, lung inflammation, host-virus interaction
MeSH terms
Animals, Cell Movement, Immunity, Innate, Inflammation, Interleukin-1, Orthomyxoviridae Infections, Influenza A virus, Pneumonia, Sympathectomy, Sympathetic Nervous System, Survival Rate, Cytokines, Mice

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