Phagocyte-derived catecholamines enhance acute inflammatory injury
Open accessAbstract
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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Any source of alveolar injury and inflammation, whether direct or indirect, can trigger a cascade of inflammation leading to increased concentrations of intra-alveolar catecholamines, which in turn promote the growth and virulence of select bacterial community members and a disordered bacterial community that perpetuates alveolar inflammation.
“Thus any source of alveolar injury and inflammation, whether direct (eg, aspiration or ventilator-induced lung injury60) or indirect (eg, sepsis or shock) can trigger a cascade of inflammation leading to increased concentrations of intra-alveolar catechol amines,120 which in turn promote the growth and virulence of select bacterial community members and a disordered bacterial community that perpet”
From The microbiome and critical illness (2016) · cites this paper as [120]
This inflammatory effect was accompanied by objective sleep impairments, indicated by a decrease in sleep duration (actigraphy) of 45 min daily in those suffering from insomnia disorder.
“This inflammatory effect was accompanied by objective sleep impairments, as indicated by a decrease in sleep duration (as measured by actigraphy) of 45 min daily in those suffering from insomnia disorder”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [191]
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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
- Venue
- Nature
- Published
- 2007-09-30
- Volume
- 449
- Issue
- 7163
- Pages
- 721-725
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- 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
- Health Sciences › Medicine › Psychiatry and Mental health › 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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