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Microglia are the major cellular source of inducible nitric oxide synthase during experimental herpes encephalitis

Cristina P Marques1, Maxim C-J Cheeran, Joseph M Palmquist

  • 1Neuroimmunology Laboratory, Center for Infectious Diseases and Microbiology Translational Research, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA.

Journal of Neurovirology
|June 24, 2008
PubMed

Insights

Overproduction of reactive nitrogen and oxygen species (RNS and ROS) contributes to brain damage during herpes encephalitis. Microglia are identified as a major source of inducible nitric oxide synthase (iNOS) in infected brains.

Area of Science:

  • Neuroimmunology
  • Infectious Diseases
  • Oxidative Stress

Background:

  • Reactive nitrogen and oxygen species (RNS and ROS) play a dual role in viral infections, acting as innate defenses but also causing damage.
  • Herpes simplex virus type 1 (HSV-1) encephalitis can lead to significant neuropathology.
  • Oxidative stress is implicated in the pathogenesis of various neurological disorders.

Purpose of the Study:

  • To investigate the role of oxidative stress in herpes encephalitis.
  • To examine the expression kinetics of inducible nitric oxide synthase (iNOS) and heme oxygenase-1 (HO-1) during HSV-1 infection.
  • To identify the cellular sources of iNOS in the infected brain.

Main Methods:

  • Gene expression analysis of iNOS and HO-1 in infected mouse brains.
  • Real-time bioluminescence imaging of HO-1 promoter activity in transgenic mice.
  • Immunohistochemistry for 3-nitrotyrosine and 8-hydroxydeoxyguanosine (8-OH-dG).
  • Quantification of 8-isoprostane levels.
  • Fluorescence-activated cell sorting (FACS) of brain leukocytes.

Main Results:

  • Both iNOS and HO-1 gene expression were significantly elevated in the brain from 7 to 21 days post-infection (d.p.i.).
  • HO-1 promoter activity was detected early (3 d.p.i.) and peaked between 5-7 d.p.i. in infected mice.
  • Evidence of oxidative brain damage was confirmed by elevated 3-nitrotyrosine, 8-OH-dG, and 8-isoprostane levels.
  • Resident microglia (CD45(int)/CD11b(+)) were identified as the primary cellular source of iNOS expression.

Conclusions:

  • Oxidative stress and iNOS expression are significantly upregulated during herpes encephalitis.
  • Microglia play a key role in the inflammatory response and oxidative damage in HSV-1 encephalitis.
  • These findings highlight the immunopathologic contribution of oxidative stress in herpes encephalitis.

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