Fig. 1

Hypoxic pre-conditioning reduces the severity of EAE both clinically and histopathologically. a. The impact of chronic mild hypoxia (CMH) on clinical severity in EAE. The progression of EAE in mice maintained under normoxic (control) or CMH conditions was evaluated by measuring clinical score at daily intervals. All points represent the mean ± SD (n = 15 mice per group, representative of 4 separate experiments). Note that compared to normoxic mice, CMH markedly reduced clinical score both at the peak of disease activity and at all time-points thereafter for the duration of the experiment (7 weeks), resulting in a marked and sustained reduction in long-term clinical score. b, e and f. Frozen sections of lumbar spinal cord taken from disease-free, EAE-normoxia or EAE-CMH mice at the peak symptomatic phase of EAE (14–15 days post-immunization) were stained for the inflammatory leukocyte marker CD45 (AlexaFluor-488) and fluoromyelin-red (FM) in panels B (scale bar = 500 μm) and E (scale bar = 100 μm) or CD4 in panel F (scale bar = 100 μm). Quantification of CD45 (c), fluoromyelin (d) and CD4 (g) fluorescent signal at peak phase of EAE. Results are expressed as the mean ± SEM (n = 6 mice/group). Note that CMH markedly suppressed CD45+ and CD4+ leukocyte infiltration and protected against demyelination. In panel B asterisks mark the zones of demyelination. ** p < 0.01