JCI - Heme oxygenase–1 and carbon monoxide suppress autoimmune neuroinflammation

Heme oxygenase–1 and carbon monoxide suppress autoimmune neuroinflammation

Ângelo A. Chora, Paulo Fontoura, Andreia Cunha, Teresa F. Pais, Sílvia Cardoso, Peggy P. Ho, Lowen Y. Lee, Raymond A. Sobel, Lawrence Steinman, Miguel P. Soares

Published in Volume 117, Issue 2

J Clin Invest. 2007; 117(2):438–447 doi:10.1172/JCI28844

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Figure 1

HO-1 and CO suppress EAE progression.

EAE was induced, and disease severity was scored daily thereafter. Clinical scores are shown as mean ± SEM. (A) Progression of EAE in C57BL/6 Hmox1^+/+ (open circles; n = 21) versus Hmox1^–/– (filled circles; n = 8) mice. (B and C) C57BL/6 (B) or SJL/J (C) mice, randomized 2 days after EAE onset, were treated daily with PBS (open squares; n = 10–15), CoPPIX (filled squares; n = 10–14), or ZnPPIX (gray squares; n = 10–14). (D) C57BL/6 Hmox1^+/+ mice were treated as in B. Hmox1 mRNA and protein expression in the CNS were assessed by quantitative RT-PCR and Western blotting, respectively. Hmox1 mRNA expression is shown as mean number of Hmox1 per HPRT mRNA molecules ± SD. (E) EAE was induced in C57BL/6 Hmox1^+/+ (open circles; n = 12) and Hmox1^–/– (filled circles; n = 3) mice treated with CoPPIX as in B. (F) EAE was induced in C57BL/6 Hmox1^+/+ mice, randomized 10–12 days after immunization, and exposed to CO (450 ppm; dark gray squares; n = 20) or not (light gray squares; n = 22). Shaded areas indicate periods of designated treatment. *P < 0.05; **P < 0.01.