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Sequential expression of mRNA for proinflammatory cytokines and interleukin‐10 in the rat peripheral nervous system: Comparison between immune‐mediated demyelination and wallerian degeneration
Author(s) -
Gillen Clemens,
Jander Sebastian,
Stoll Guido
Publication year - 1998
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19980215)51:4<489::aid-jnr8>3.0.co;2-8
Subject(s) - proinflammatory cytokine , wallerian degeneration , medicine , interleukin , immune system , immunology , messenger rna , interleukin 10 , downregulation and upregulation , biology , cytokine , inflammation , pathology , biochemistry , gene
This study examined the time course of mRNA levels of the proinflammatory cytokines interferon‐γ (IFNγ), interleukin‐1β (IL1β), interleukin‐12 (IL12; p40 subunit), and the immunosuppressant interleukin‐10 (IL10) by semiquantitative reverse transcription polymerase chain reaction (RT‐PCR) in rats with actively induced experimental autoimmune neuritis (EAN) and in distal stumps of crushed sciatic nerves undergoing Wallerian degeneration. In EAN IFNγ‐ and IL1β‐mRNA peaked at the onset and acute phase of clinical disease. IL12p40‐mRNA was upregulated later than IFNγ‐mRNA in the late acute phase from days 15 to 21. IL10‐mRNA appeared concomitantly with the proinflammatory cytokines at day 11, but persisted at high levels into the clinical recovery phase. After nerve crush both IL1β‐ and IL10‐mRNA were rapidly upregulated in the distal stump at day 1 and slowly declined over the next 2 weeks. Significant levels of mRNA for IFNγ could be found at days 4 and 7, whereas IL12p40‐mRNA showed a biphasic induction. We provide evidence for a concomitant induction of pro‐ and anti‐inflammatory cytokines in EAN. Moreover, the rapid upregulation in Wallerian degeneration suggests a more general role of cytokines in the biology of the peripheral nerve. J. Neurosci. Res. 51:489–496, 1998. © 1998 Wiley‐Liss, Inc.