| Item type: | Article | ||||
|---|---|---|---|---|---|
| Journal or Publication Title: | Brain, Behavior, and Immunity | ||||
| Publisher: | ACADEMIC PRESS INC ELSEVIER SCIENCE | ||||
| Place of Publication: | SAN DIEGO | ||||
| Volume: | 46 | ||||
| Page Range: | pp. 180-191 | ||||
| Date: | 2015 | ||||
| Institutions: | Medicine > Lehrstuhl für Innere Medizin I Medicine > Lehrstuhl für Orthopädie | ||||
| Identification Number: |
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| 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 | ||||
| Dewey Decimal Classification: | 600 Technology > 610 Medical sciences Medicine | ||||
| Status: | Published | ||||
| Refereed: | Yes, this version has been refereed | ||||
| Created at the University of Regensburg: | Yes | ||||
| Item ID: | 60463 |
Web of ScienceAbstract
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 ...
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.
Metadata last modified: 19 Dec 2024 07:34
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