Astrocytes and microglia express inducible nitric oxide synthase in mice with experimental allergic encephalomyelitis

J Neuroimmunol. 1997 Apr;74(1-2):121-9. doi: 10.1016/s0165-5728(96)00215-9.


Nitric oxide (NO), produced by inducible NO synthase (iNOS), may play a role in inflammatory demyelinating diseases of the central nervous system (CNS). We show upregulation of iNOS mRNA in CNS of SJL/J mice with experimental allergic encephalomyelitis (EAE). Using antibodies against mouse iNOS, GFAP (a marker for astrocytes) and Mac-1/CD11b (a marker for macrophages/microglia), both astrocytes and macrophages/microglia were identified as iNOS-expressing cells in situ in EAE lesions. GFAP + astrocytes not associated with inflammatory infiltrates were also found to express iNOS. Because microglia rather than astrocytes are implicated in demyelinating pathology, we propose that microglial NO may be cytopathic whereas astrocyte-derived NO may be protective in EAE.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Astrocytes / enzymology*
  • Astrocytes / metabolism
  • Central Nervous System / cytology
  • Central Nervous System / enzymology
  • Central Nervous System / physiopathology
  • Encephalomyelitis, Autoimmune, Experimental / enzymology*
  • Encephalomyelitis, Autoimmune, Experimental / genetics
  • Enzyme Induction
  • Female
  • Gene Expression
  • Glial Fibrillary Acidic Protein / metabolism
  • Mice
  • Mice, Inbred Strains
  • Microglia / enzymology*
  • Nitric Oxide Synthase / genetics
  • Nitric Oxide Synthase / metabolism*
  • Tissue Distribution


  • Glial Fibrillary Acidic Protein
  • Nitric Oxide Synthase