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Cyclo-oxygenases and prostaglandins in acute inflammatory demyelination of the peripheral nerve

From the Department of Neurology, Research Group for Clinical and Experimental Neuroimmunology (Drs. Hu, Hartung, and Kieseier), Heinrich-Heine University, Düsseldorf, Germany; and Neuroscience Unit, School of Biological Sciences (Dr. Mathey), University of Sydney, Australia.

Address correspondence and reprint requests to Dr. Bernd C. Kieseier, Department of Neurology, Research Group for Clinical and Experimental Neuroimmunology, Heinrich-Heine University, Moorenstrasse 5, 40225 Düsseldorf, Germany; e-mail: bernd.kieseier{at}uni-duesseldorf.de

Objective: To investigate the expression of cyclo-oxygenases (COX), key enzymes in propagating inflammatory responses by converting arachidonic acid to prostaglandins, in inflammatory demyelinating disorders of the peripheral nervous system (PNS).

Methods: Expression and distribution of COX messenger RNA (mRNA) and protein were studied in sural nerve biopsies, serum, and CSF samples from patients with Guillain–Barré syndrome (GBS), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), or, for comparison, with vasculitic neuropathy (VN), which is a inflammatory nondemyelinating disorder, and noninflammatory neuropathies (NIN) using RT-PCR, immunohistochemistry, and immunoblotting. To confirm functional COX-2 activity, the expression of prostaglandin E₂ (PGE₂) and prostaglandin F₂ (PGF₂) was evaluated by ELISA ex vivo and in vitro.

Results: Whereas COX-1 expression was unaltered in all investigated groups, a significant upregulation of COX-2 mRNA was detected in sural nerves from patients with GBS, CIDP, or VN but not in control subjects with noninflammatory disorders. Macrophages were identified as its primary cellular source. Increased COX-2 protein levels were detectable in serum and CSF from all patients with GBS and, in smaller numbers only, in samples from patients with CIDP or VN but not from the NIN group studied. Moreover, increased levels of PGE₂ and PGF₂ were measurable in sera from patients with GBS, CIDP, or VN and in cell culture supernatants from in vitro stimulated macrophages, indicative of COX-2 activity.

Conclusions: Cyclo-oxygenase-2, expressed by macrophages, may generate prostaglandins during acute inflammatory demyelination of the peripheral nerve.

Received March 14, 2003. Accepted in final form August 27, 2003.

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