Differential expression of interleukin-10 mRNA in Wallerian degeneration and immune-mediated inflammation of the rat peripheral nervous system

• Published in: Journal of neuroscience research Vol. 43; no. 2; pp. 254 - 259
• Main Authors: Jander, S., Pohl, J., Gillen, C., Stoll, G.
• Format: Journal Article
• Language: English
• Published: New York John Wiley & Sons, Inc 15.01.1996
• Subjects: Animals; axotomy; DNA Probes; experimental autoimmune neuritis; Female; Immunohistochemistry; In Situ Hybridization; Interleukin-10 - biosynthesis; macrophage; Macrophages - drug effects; Macrophages - metabolism; Neuritis - immunology; Neuritis - metabolism; Neuritis - pathology; Peripheral Nervous System - metabolism; Peripheral Nervous System - pathology; Rats; Rats, Inbred Lew; RNA, Messenger - biosynthesis; Schwann cell; Schwann Cells - drug effects; Schwann Cells - metabolism; Wallerian Degeneration - drug effects
• ISSN: 0360-4012; 1097-4547
• DOI: 10.1002/(SICI)1097-4547(19960115)43:2<254::AID-JNR13>3.0.CO;2-6

Interleukin‐10 (IL‐10) is a potent immunosuppressant cytokine which downregulates MHC class II antigen expression and inflammatory cytokine production. In this study we localized mRNA for IL‐10 in the rat peripheral nervous system (PNS) by nonradioactive in situ hybridization using a digoxygenin‐labeled riboprobe specific for rat IL‐10. IL‐10 mRNA was expressed by some Schwann cells (SCs) in the normal sciatic nerve. During Wallerian degeneration, SCs strongly expressed IL‐10 mRNA between days 2 and 4 after transection. By day 14 only occasional cells were positive for IL‐10 mRNA. The vast majority of ED1‐positive macrophages were IL‐10 negative after axotomy. Contrastingly, infiltrating macrophages expressed IL‐10 mRNA coincident with beginning clinical recovery in experimental autoimmune neuritis (EAN), the rat model of human Guillain‐Barré syndrome. Our data suggest that SCs provide a constitutive immunosuppressant system in the PNS. In EAN additional macrophage‐derived IL‐10 may be important for the resolution of the T cell‐mediated immune response. © 1996 Wiley‐Liss, Inc.