Fig. 6

CD36 inhibition increases neuroinflammation and disease severity in the experimental autoimmune encephalomyelitis animal model. a Disease score of 12-week-old wild-type (wt) mice in which experimental autoimmune encephalomyelitis (EAE) was induced. Starting 9 days post-immunization, animals were injected intraperitoneally with vehicle (n = 9 animals) or the CD36 inhibitor sulfo-N-succinimidyl oleate (SSO, 30 mg/kg, n = 10 animals) on a daily basis. b–d Quantification and representative images of an Oil Red O (ORO) staining (b, d, n = 6 lesions) and degenerated myelin (dMBP) staining (c, d, n = 5 animals) of spinal cord tissue obtained from EAE animals treated with vehicle or CD36 inhibitor. Dotted line delineates the circumference of the lesion. Lesion lipid and myelin debris load are defined as the percentage of lesion area that is ORO⁺ and dMBP⁺, respectively. Scale bars, 100 μm; 25 μm (inlet images). e Quantification of F4/80 staining of spinal cord tissue obtained from EAE animals treated with vehicle or CD36 inhibitor (n = 5 animals). f Flow cytometric analysis of intracellular lipid load (BODIPY stain) in CD45⁺ leukocytes (n = 4 animals). Data are depicted as mean fluorescence intensity (MFI). g Quantitative PCR was used to assess mRNA expression of Il1b, Nos2, Tnfa, Il6, Ccl4, and Ccl5 spinal cord tissue obtained from EAE animals treated with vehicle or CD36 inhibitor (n = 6 animals). h, i Quantification and representative images of NOS2/F4/80 staining of spinal cord tissue obtained from EAE animals treated with vehicle or CD36 inhibitor (n = 5 animals). Phagocyte NOS2 abundance is defined as the NOS2 MFI of F4/80⁺ cells. Scale bar, 25 μm. Data are represented as mean ± s.e.m. *p < 0.05, **p < 0.01, and ***p < 0.001