title: Bioluminescence in vivo imaging of autoimmune encephalomyelitis predicts disease.
abstract: BACKGROUND
  Experimental autoimmune encephalomyelitis is a widely used animal model to understand not only multiple sclerosis but also basic principles of immunity. The disease is scored typically by observing signs of paralysis, which do not always correspond with pathological changes.
  
  
  METHODS
  Experimental autoimmune encephalomyelitis was induced in transgenic mice expressing an injury responsive luciferase reporter in astrocytes (GFAP-luc). Bioluminescence in the brain and spinal cord was measured non-invasively in living mice. Mice were sacrificed at different time points to evaluate clinical and pathological changes. The correlation between bioluminescence and clinical and pathological EAE was statistically analyzed by Pearson correlation analysis.
  
  
  RESULTS
  Bioluminescence from the brain and spinal cord correlates strongly with severity of clinical disease and a number of pathological changes in the brain in EAE. Bioluminescence at early time points also predicts severity of disease.
  
  
  CONCLUSIONS
  These results highlight the potential use of bioluminescence imaging to monitor neuroinflammation for rapid drug screening and immunological studies in EAE and suggest that similar approaches could be applied to other animal models of autoimmune and inflammatory disorders.
authors.affiliation: Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA. jianl@stanford.edu
authors.forename: Jian
authors.initials: J
authors.lastname: Luo
authors.forename: Peggy
authors.initials: P
authors.lastname: Ho
authors.forename: Lawrence
authors.initials: L
authors.lastname: Steinman
authors.forename: Tony
authors.initials: T
authors.lastname: Wyss-Coray
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D001921:Brain / Q000378:metabolism / Q000473:pathology; D015704:CD4 Antigens / Q000378:metabolism; D003952:Diagnostic Imaging / Q000379:methods*; D004195:Disease Models, Animal; D018450:Disease Progression; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000139:chemically induced / Q000175:diagnosis* / Q000378:metabolism; D005904:Glial Fibrillary Acidic Protein / Q000235:genetics; D006023:Glycoproteins; D008156:Luciferases / Q000096:biosynthesis / Q000235:genetics; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D063308:Myelin-Oligodendrocyte Glycoprotein; D010446:Peptide Fragments; D012720:Severity of Illness Index; D013116:Spinal Cord / Q000378:metabolism / Q000473:pathology; D013997:Time Factors; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D015704:CD4 Antigens; D005904:Glial Fibrillary Acidic Protein; D006023:Glycoproteins; D008156:Luciferases; D063308:Myelin-Oligodendrocyte Glycoprotein; D010446:Peptide Fragments; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C445081:myelin oligodendrocyte glycoprotein (35-55)