Neuroimmune interactions are known to influence several chronic inflammatory and
rheumatic diseases, but the underlying mechanisms have been insufficiently elucidated. The cholinergic anti-inflammatory pathway is characterized by neural regulation of systemic
inflammation, mediated by the vagus nerve and specific
cholinergic stimulation of the nicotinic alpha-7
acetylcholine receptor (
alpha7nAChR) on immune cells. Moreover,
alpha7nAChR has been shown important for immune regulation also in the absence of nerves, but little is known about these mechanisms in chronic joint
inflammation. The expression and localization of
alpha7nAChR in synovial biopsies from patients with
rheumatoid arthritis and
psoriatic arthritis was investigated by immunohistochemistry using
monoclonal antibody against
alpha7nAChR. Surface staining of
alpha7nAChR was observed in synovial tissue of all
arthritis patients investigated and could also to a lesser extent be detected in the synovium of healthy individuals.
alpha7nAChR positive cells were detected in mainly synovial lining cells and vessels. The
alpha7nAChR positively stained cells were by double immunofluorescence identified as primarily macrophages and fibroblasts, with the majority of these cells expressing the receptor. These results indicate the importance of
alpha7nAChR and
cholinergic mechanisms in
arthritis pathogenesis and implicate specific
cholinergic modulation as a potential anti-inflammatory therapeutic strategy in joint
inflammation.