PMID- 11494369
OWN - NLM
STAT- MEDLINE
DCOM- 20010913
LR  - 20061115
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 65
IP  - 4
DP  - 2001 Aug 15
TI  - Induction of the proinflammatory cytokine interleukin-18 by axonal injury.
PG  - 332-9
AB  - Interleukin-18 (IL-18) is an important cytokine in innate immunity and in the 
      induction phase of autoimmunity. We report the expression of IL-18 mRNA and 
      protein after nerve crush during Wallerian degeneration (WD) of the rat nervous 
      system. In normal optic nerves (ON) constitutive IL-18 mRNA levels as revealed by 
      semiquantitative reverse transcriptase polymerase chain reaction were higher than 
      in sciatic nerves (SN). After nerve crush, steady-state levels moderately 
      increased in the distal nerve part of the SN but not the ON. By 
      immunocytochemistry no SN or faint ON IL-18 protein expression was detectable in 
      normal nerves. In contrast, IL-18 expression dramatically increased after SN and 
      ON crush. On the cellular level, ED1(+) macrophages infiltrating the crush site 
      strongly expressed IL-18 at days 2 and 4 after SN crush. By days 4 and 8, in 
      addition, the entire distal nerve part was covered by IL-18(+) macrophages. At 
      day 16, IL-18 immunoreactivity had disappeared despite the persistence of large 
      numbers of ED1(+) macrophages. A similar infiltration of IL-18(+) macrophages was 
      seen at the crush site in the ON. Moreover, microglia in the distal ON stump 
      lacking macrophage infiltration and undergoing delayed myelin degradation 
      up-regulated IL-18. In conclusion this study shows that IL-18 is involved in the 
      cytokine network associated with the robust inflammatory response during WD of 
      the SN. Despite up-regulation of the proinflammatory cytokine IL-18, major 
      histocompatibility complex class II, and CD4 molecules similar to macrophages in 
      the PNS, microglial activation after ON injury appears to be insufficient to 
      mount an effective phagocytic response as a prerequisite for successful 
      regeneration in the CNS.
CI  - Copyright 2001 Wiley-Liss, Inc.
FAU - Menge, T
AU  - Menge T
AD  - Department of Neurology, Heinrich-Heine-Universitat, Dusseldorf, Germany.
FAU - Jander, S
AU  - Jander S
FAU - Stoll, G
AU  - Stoll G
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Interleukin-18)
RN  - 0 (RNA, Messenger)
RN  - EC 3.4.22.36 (Caspase 1)
SB  - IM
MH  - Animals
MH  - Axons/*immunology/pathology
MH  - Caspase 1/genetics
MH  - Female
MH  - Gene Expression/immunology
MH  - Interleukin-18/*genetics/*immunology
MH  - Macrophages/immunology
MH  - Microglia/immunology
MH  - Nerve Crush
MH  - Nerve Regeneration/*immunology
MH  - Optic Nerve Injuries/immunology/pathology
MH  - RNA, Messenger/analysis
MH  - Rats
MH  - Rats, Wistar
MH  - Sciatic Nerve/immunology/injuries/pathology
MH  - Wallerian Degeneration/immunology/pathology
EDAT- 2001/08/09 10:00
MHDA- 2001/09/14 10:01
CRDT- 2001/08/09 10:00
PHST- 2001/08/09 10:00 [pubmed]
PHST- 2001/09/14 10:01 [medline]
PHST- 2001/08/09 10:00 [entrez]
AID - 10.1002/jnr.1158 [doi]
PST - ppublish
SO  - J Neurosci Res. 2001 Aug 15;65(4):332-9. doi: 10.1002/jnr.1158.