Cited by 475Vagus Nerve Stimulation ResearchCancer, Stress, Anesthesia, and Immune ResponseInflammation biomarkers and pathways

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Phagocyte-derived catecholamines enhance acute inflammatory injury

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Flierl, Michael A., Rittirsch, Daniel, Nadeau, Brian A., Chen, Anthony J., Sarma, J. Vidya, Zetoune, Firas S., McGuire, Stephanie R., List, Rachel P., Day, Danielle E., Hoesel, L. Marco, Gao, Hongwei, Van Rooijen, Nico, Huber-Lang, Markus S., Neubig, Richard R., Ward, Peter A.·2007·Nature

DOI 10.1038/nature06185

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Abstract

It is becoming increasingly clear that the autonomic nervous system and the immune system demonstrate cross-talk during inflammation by means of sympathetic and parasympathetic pathways. We investigated whether phagocytes are capable of de novo production of catecholamines, suggesting an autocrine/paracrine self-regulatory mechanism by catecholamines during inflammation, as has been described for lymphocytes. Here we show that exposure of phagocytes to lipopolysaccharide led to a release of catecholamines and an induction of catecholamine-generating and degrading enzymes, indicating the presence of the complete intracellular machinery for the generation, release and inactivation of catecholamines. To assess the importance of these findings in vivo, we chose two models of acute lung injury. Blockade of alpha2-adrenoreceptors or catecholamine-generating enzymes greatly suppressed lung inflammation, whereas the opposite was the case either for an alpha2-adrenoreceptor agonist or for inhibition of catecholamine-degrading enzymes. We were able to exclude T cells or sympathetic nerve endings as sources of the injury-modulating catecholamines. Our studies identify phagocytes as a new source of catecholamines, which enhance the inflammatory response.

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Authors: Flierl, M. A., Rittirsch, D., Nadeau, B. A., Chen, A. J., Sarma, J. V., Zetoune, F. S., McGuire, S. R., List, R. P., Day, D. E., Hoesel, L. M., Gao, H., Van Rooijen, N., Huber-Lang, M. S., Neubig, R. R., & Ward, P. A.
Affiliations: University of Michigan (US)
Universität Ulm (DE)
Corresponding author: Ward, Peter A.
ORCID: Flierl, Michael A.
Rittirsch, Daniel
Nadeau, Brian A.
Gao, Hongwei
Huber-Lang, Markus S.
Neubig, Richard R.
Ward, Peter A.
Venue: Nature
Publisher: Springer Science and Business Media LLC
Published: 2007-09-30
Volume: 449
Issue: 7163
Pages: 721-725
ISSN: 0028-0836 (ISSN-L)
1476-4687
DOI: 10.1038/nature06185
OpenAlex: W2058021161
Cited by: 475
References: 26
Citations by year: 2026: 17 · 2025: 18 · 2024: 26 · 2023: 16 · 2022: 24 · 2021: 25 · 2020: 29 · 2019: 35 · 2018: 26 · 2017: 22 · 2016: 26 · 2015: 34 · 2014: 20 · 2013: 27 · 2012: 22
FWCI: 14.58
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.springer.com/tdm (tdm)
Locations: Nature (publishedVersion)
PubMed (publishedVersion)
Deep Blue (University of Michigan) (submittedVersion)
RePEc: Research Papers in Economics (submittedVersion)
Funders: Deutsche Forschungsgemeinschaft
National Institutes of Health
Topics: Life Sciences › Neuroscience › Neurology › Vagus Nerve Stimulation Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Stress, Anesthesia, and Immune Response
Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
Keywords: phagocytes, catecholamines, norepinephrine, epinephrine, acute lung injury, macrophages, neutrophils, lipopolysaccharide, alpha2-adrenoceptors, adrenergic system, neuroimmune interactions, autocrine and paracrine regulation, inflammatory injury
MeSH terms: Acute Disease, Animals, Catecholamines, Inflammation, Lipopolysaccharides, Lung Diseases, Macrophages, Male, Neutrophils, Phagocytes, T-Lymphocytes, Receptors, Adrenergic, alpha-2, Rats, Long-Evans, Rats, Adrenergic alpha-2 Receptor Antagonists

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Phagocyte-derived catecholamines enhance acute inflammatory injury

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