Phagocyte-derived catecholamines enhance acute inflammatory injury
Michael A. Flierl,
Daniel Rittirsch,
Brian A. Nadeau,
Anthony J. Chen,
J. Vidya Sarma,
Firas S. Zetoune,
Stephanie R. McGuire,
Rachel P. List,
Danielle E. Day,
L. Marco Hoesel,
Hongwei Gao,
Nico Van Rooijen,
Markus S. Huber-Lang,
Richard R. Neubig and
Peter A. Ward ()
Additional contact information
Michael A. Flierl: Department of Pathology,
Daniel Rittirsch: Department of Pathology,
Brian A. Nadeau: Department of Pathology,
Anthony J. Chen: Department of Pathology,
J. Vidya Sarma: Department of Pathology,
Firas S. Zetoune: Department of Pathology,
Stephanie R. McGuire: Department of Pathology,
Rachel P. List: Department of Pathology,
Danielle E. Day: Department of Pathology,
L. Marco Hoesel: Department of Pathology,
Hongwei Gao: Department of Pathology,
Nico Van Rooijen: Vrije Universiteit
Markus S. Huber-Lang: Hand- and Reconstructive Surgery, University of Ulm Medical School
Richard R. Neubig: University of Michigan Medical School, Ann Arbor, Michigan 48109, USA
Peter A. Ward: Department of Pathology,
Nature, 2007, vol. 449, issue 7163, 721-725
Abstract:
Adrenergic inflammation The discovery that phagocytic blood cells (macrophages and neutrophils) are a significant source of catecholamines (noradrenaline and adrenaline), and can cause reinforcement of the acute inflammatory response, comes as a surprise. The body's inflammatory response to traumatic injury or infection is designed to protect it and return it to the preinjury state, but excessive inflammatory responses can seriously injure tissues and organs. Experiments in rat and mouse models of acute lung injury show that phagocytes act as virtually a third component of the adrenergic system — joining the adrenal medulla in the brain, and synaptic neurons. The findings raise the possibility that unwanted inflammatory responses (as seen in atherosclerosis, acute cardiac ischaemic injury and acute lung injury) might be suppressed in humans by adrenoreceptor blockade.
Date: 2007
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Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:449:y:2007:i:7163:d:10.1038_nature06185
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DOI: 10.1038/nature06185
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