Abstract
The loss of sympathetic nerve fibers (SNF) is a general principle in inflammatory diseases. Since sympathetic neurotransmitters exert anti-inflammatory effects at increased concentrations, their loss in inflammed and infected tissue is reasonable to overcome infection. However, this mechanism is unfavourable in chronic inflammation like rheumatoid arthritis (RA). Semaphorins are major factors involved in axon guidance and repulsion mediated by a neuropilin-2/plexin A2 receptor complex on nerve endings. We hypothesize that antagonizing semaphorin binding to its receptor can keep nerve fibers in the inflamed area, and this may be a new therapeutic principle in the treatment of RA. In this study, we wanted to test the neutralizing effects of polyclonal antibodies to plexin A2 on semaphorin 3F-induced nerve fiber repulsion. For these investigations, a neurite outgrowth assay was used to study the behaviour of nerve fibers from sympathetic trunk ganglia of postnatal mice. Nerve repulsion caused by semaphorin 3F is about 35–50%. Repulsion can be completely abrogated by a polyclonal anti-plexin A2 antibody in a concentration of 157 nmol/l (to 0–9%; p This study provided us with a first important tool to manipulate sympathetic nerve fiber repulsion. We are testing these antibodies in an animal model of experimental arthritis.
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