Sympathetic nervous system controls resolution of inflammation via regulation of repulsive guidance molecule A

Andreas Körner, Martin Schlegel, Torsten Kaussen, Verena Gudernatsch, Georg Hansmann, Timo Schumacher, Martin Giera and Valbona Mirakaj ()
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Andreas Körner: University Hospital Tübingen, Eberhard-Karls University
Martin Schlegel: University Hospital Tübingen, Eberhard-Karls University
Torsten Kaussen: Department of Pediatric Cardiology and Critical Care
Verena Gudernatsch: University Hospital Tübingen, Eberhard-Karls University
Georg Hansmann: Department of Pediatric Cardiology and Critical Care
Timo Schumacher: Department of Pediatric Cardiology and Critical Care
Martin Giera: Leiden University Medical Center (LUMC)
Valbona Mirakaj: University Hospital Tübingen, Eberhard-Karls University

Nature Communications, 2019, vol. 10, issue 1, 1-15

Abstract: Abstract The bidirectional communication between the immune and nervous system is important in regulating immune responses. Here we show that the adrenergic nerves of sympathetic nervous system orchestrate inflammation resolution and regenerative programs by modulating repulsive guidance molecule A (RGM-A). In murine peritonitis, adrenergic nerves and RGM-A show bidirectional activation by stimulating the mutual expression and exhibit a higher potency for the cessation of neutrophil infiltration; this reduction is accompanied by increased pro-resolving monocyte or macrophage recruitment, polymorphonucleocyte clearance and specialized pro-resolving lipid mediators production at sites of injury. Chemical sympathectomy results in hyperinflammation and ineffective resolution in mice, while RGM-A treatments reverse these phenotypes. Signalling network analyses imply that RGM-A and β2AR agonist regulate monocyte activation by suppressing NF-κB activity but activating RICTOR and PI3K/AKT signalling. Our results thus illustrate the function of sympathetic nervous system and RGM-A in regulating resolution and tissue repair in a murine acute peritonitis model.

Date: 2019
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DOI: 10.1038/s41467-019-08328-5

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