Neutrophil-derived catecholamines mediate negative stress effects on bone

Miriam E. A. Tschaffon-Müller, Elena Kempter, Lena Steppe, Sandra Kupfer, Melanie R. Kuhn, Florian Gebhard, Carlos Pankratz, Miriam Kalbitz, Konrad Schütze, Harald Gündel, Nele Kaleck, Gudrun Strauß, Jean Vacher, Hiroshi Ichinose, Katja Weimer, Anita Ignatius, Melanie Haffner-Luntzer and Stefan O. Reber ()
Additional contact information
Miriam E. A. Tschaffon-Müller: Ulm University Medical Center
Elena Kempter: Ulm University Medical Center
Lena Steppe: Ulm University Medical Center
Sandra Kupfer: Ulm University Medical Center
Melanie R. Kuhn: Ulm University Medical Center
Florian Gebhard: Ulm University Medical Center
Carlos Pankratz: Ulm University Medical Center
Miriam Kalbitz: Ulm University Medical Center
Konrad Schütze: Ulm University Medical Center
Harald Gündel: Ulm University Medical Center
Nele Kaleck: Ulm University Medical Center
Gudrun Strauß: Ulm University Medical Center
Jean Vacher: Institut de Recherches Cliniques de Montréal
Hiroshi Ichinose: Tokyo Institute of Technology
Katja Weimer: Ulm University Medical Center
Anita Ignatius: Ulm University Medical Center
Melanie Haffner-Luntzer: Ulm University Medical Center
Stefan O. Reber: Ulm University Medical Center

Nature Communications, 2023, vol. 14, issue 1, 1-15

Abstract: Abstract Mental traumatization is associated with long-bone growth retardation, osteoporosis and increased fracture risk. We revealed earlier that mental trauma disturbs cartilage-to-bone transition during bone growth and repair in mice. Trauma increased tyrosine hydroxylase-expressing neutrophils in bone marrow and fracture callus. Here we show that tyrosine hydroxylase expression in the fracture hematoma of patients correlates positively with acknowledged stress, depression, and pain scores as well as individual ratings of healing-impairment and pain-perception post-fracture. Moreover, mice lacking tyrosine hydroxylase in myeloid cells are protected from chronic psychosocial stress-induced disturbance of bone growth and healing. Chondrocyte-specific β2-adrenoceptor-deficient mice are also protected from stress-induced bone growth retardation. In summary, our preclinical data identify locally secreted catecholamines in concert with β2-adrenoceptor signalling in chondrocytes as mediators of negative stress effects on bone growth and repair. Given our clinical data, these mechanistic insights seem to be of strong translational relevance.

Date: 2023
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DOI: 10.1038/s41467-023-38616-0

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