The Role of Kinin Receptors in Preventing Neuroinflammation and Its Clinical Severity during Experimental Autoimmune Encephalomyelitis in Mice
Figure 3
The blockade of kinin B1R in the disease induction phase by pharmacological treatment or genetic deletion ameliorated EAE pathology.
The spinal lumbar cords obtained on the 25th day after immunization from the different experimental groups were processed for immunohistochemistry assays: T cell infiltration by CD3 immunoreactivity (A–F); astrocytes activation by GFAP immunoreactivity (G–L); and CREB phosphorylation (M–R). Specifically, four 5-µm sections of lumbar spinal cord white matter (six to nine mice/group)≈150 µm apart were obtained between L4 and L6 from the naive group (A, G and M), the EAE group (B, H and N), from mice pre-treated with the B1R antagonist DALBK (50 nmol/kg) (C, I and O), from mice pre-treated with the B2R antagonist HOE-140 (150 nmol/kg) (D, J and P) and from mice deficient in B1R (E, K and Q) and B2R (F, L and R). The antagonists were administered i.p. twice a day (12/12 h), during day 0–5 p.i. Representative sections from three independent experiments are shown. Scale bar corresponds to 25 µm and applies throughout.