Stangl, Hubert and Springorum, Hans-Robeit and Muschter, Dominique and Graesse, Susanne and Straub, Rainer H. (2015) Catecholaminergic-to-cholinergic transition of sympathetic nerve fibers is stimulated under healthy but not under inflammatory arthritic conditions. BRAIN BEHAVIOR AND IMMUNITY, 46. pp. 180-191. ISSN 0889-1591, 1090-2139
Full text not available from this repository. (Request a copy)Abstract
Objective: Density of sympathetic nerve fibers decreases in inflamed arthritic tissue tested by immunoreactivity towards tyrosine-hydroxylase (TH, catecholaminergic key enzyme). Since sympathetic nerve fibers may change phenotype from catecholaminergic to cholinergic (example: sweat glands), loss of nerve fibers may relate to undetectable TH. We aimed to investigate possible catecholaminergic-to-cholinergic transition of sympathetic nerve fibers in synovial tissue of animals with arthritis, and patients with rheumatoid arthritis (RA) and osteoarthritis (OA), and we wanted to find a possible transition factor. Methods: Nerve fibers were detected by immunofluorescence towards TH (catecholaminergic) and vesicular acetylcholine transporter (cholinergic). Co-culture experiments with sympathetic ganglia and lymphocytes or osteoclast progenitors were designed to find stimulators of catecholaminergic-to-cholinergic transition (including gene expression profiling). Results: In mouse joints, an increased density of cholinergic relative to catecholaminergic nerve fibers appeared towards day 35 after immunization, but most nerve fibers were located in healthy joint-adjacent skin or muscle and almost none in inflamed synovial tissue. In humans, cholinergic fibers are more prevalent in OA synovial tissue than in RA. Co-culture of sympathetic ganglia with osteoclast progenitors obtained from healthy but not from arthritic animals induced catecholaminergic-to-cholinergic transition. Osteoclast mRNA microarray data indicated that leukemia inhibitory factor (LIF) is a candidate transition factor, which was confirmed in ganglia experiments, particularly, in the presence of progesterone. Conclusion: In humans and mice, catecholaminergic-to-cholinergic sympathetic transition happens in less inflamed tissue but not in inflamed arthritic tissue. Under healthy conditions, presence of cholinergic sympathetic nerve fibers may support the cholinergic anti-inflammatory influence recently described. (C) 2015 Elsevier Inc. All rights reserved.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | COLLAGEN-INDUCED ARTHRITIS; LEUKEMIA INHIBITORY FACTOR; RECEPTOR ALPHA-7 SUBUNIT; RHEUMATOID-ARTHRITIS; NEUROTRANSMITTER PHENOTYPE; ANTIINFLAMMATORY PATHWAY; PROTEASOMAL DEGRADATION; TYROSINE-HYDROXYLASE; SYNOVIAL TISSUE; MARKED LOSS; Cholinergic sympathetic nerve fiber; Sympathetic nervous system; Arthritis; Leukemia inhibitory factor; Progesterone |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Innere Medizin I Medicine > Lehrstuhl für Orthopädie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 19 Jul 2019 13:03 |
| Last Modified: | 19 Jul 2019 13:03 |
| URI: | https://pred.uni-regensburg.de/id/eprint/5573 |
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