Table 2.
Quantification of markers for inflammation and oxidative injury in different experimental models for CNS inflammation and multiple sclerosis
| Model | Mechanism | Active lesion |
||||
|---|---|---|---|---|---|---|
| Iba-1 | p22phox | iNOS | E06 | Iron | ||
| Acute pt EAE young | CD4+ T cells | 10.90 (5.23) | 10.46 (3.66) | 2.25 (2.10) | 122 (44) | 0.00 (0.01) |
| Acute pt EAE aged | CD4+ T cells | 8.59 (4.87) | 9.10 (3.83) | 2.99 (1.62) | 130 (37) | 0.00 (0.00) |
| Chronic MOG EAE mouse | CD4+ T cells | 11.12 (17.66) | 3.28 (8.33) | 0.02 (0.56) | 185 (46) | 0.18 (0.92) |
| Chronic MOG EAE rat | CD4+ T cells + demyelinating antibodies | 9.33 (16.18) | 0.30 (3.90) | 0.01 (0.06) | 124 (172) | 0.01 (0.73) |
| CD8 EAE | CD8+ T cells | 7.58 (7.42) | 1.17 (2.53) | 0.00 (0.31) | 233 (97) | 0.05 (0.32) |
| LPS injection | Innate immunity | 6.90 (17.30) | 0.80 (3.70) | 0.02 (0.86) | 200 (35) | 0.01 (1.00) |
| Cuprizone diet | Toxic demyelination | 11.97 (7.03) | 0.04 (0.04) | 0.00 (0.00) | 130 (46) | 0.01 (0.01) |
| Coronavirus MHV-JHM encephalomyelitis | Virus, CD8+ T cells, innate immunity | 15.81 (13.16) | 3.79 (4.73) | 0.00 (0.09) | 644 (138) | 0.01 (0.70) |
| Acute MS | Unknown | 12.60 (18.86) | 8.69 (12.12) | 0.47 (2.58) | 553 (313) | b |
| NWM/NGM |
|||||||
|---|---|---|---|---|---|---|---|
| Iba-1 | p22phox | iNOS | E06 | Iron |
|||
| BG | SC | ||||||
| Young control animals | n.p. | 2.55 (1.69) | 0.00 (0.01) | 0.00 (0.00) | 125 (48) | 0.03 (0.04) | 0.01 (0.02) |
| Old control animals | n.p. | 3.28 (2.98) | 0.00 (0.01) | 0.00 (0.00) | 110 (39) | 2.94 (2.08) | 0.01 (0.02) |
| Human controls | n.p. | 4.41 (5.58) | 2.47 (1.31)a | 0.04 (0.02)a | 336 (132)a | b | b |
Quantification of Iba-1, p22phox, iNOS, oxidised phospholipids (E06) and iron staining in active lesions of different rodent models for CNS inflammation in comparison with acute MS cases and human controls. Depicted are values of median (range) derived from optical densitometry (area fraction for Iba-1, p22phox, iNOS and iron and integrated density for E06) of equally sized pictures taken under standardised conditions of the respective animal model or MS case. Bold numbers indicate a significant increase compared to control animals, or in case of MS compared to human controls, using Mann–Whitney U post hoc tests and Bonferroni–Holm correction. In case of iron staining, lesions were compared with the respective control tissue
NWM normal white matter, NGM normal grey matter, EAE experimental autoimmune encephalomyelitis, pt passive transfer, BG basal ganglia, SC spinal cord, LPS lipopolysaccharide, n.p. not present, (young control animals n = 6; old control animals n = 6; acute EAE young n = 6; acute EAE aged n = 8; chronic MOG EAE mouse n = 15; chronic MOG EAE rat n = 14; CD8 EAE n = 6; LPS injection n = 20; cuprizone diet n = 5; coronavirus encephalomyelitis n = 11; acute MS n = 7; human controls n = 6)
A significant increase compared to animal controls. Iron staining in basal ganglia (BG) was significantly increased in old compared with young controls
Iron accumulation in MS and human controls was not quantified in the present study, as it is dependent on location and age as described elsewhere [35]