Fig. 2: EphA2 deficiency augments S. suis-induced disruption of blood brain barrier in vitro and in vivo. | Communications Biology

Fig. 2: EphA2 deficiency augments S. suis-induced disruption of blood brain barrier in vitro and in vivo.

From: Dcaf15-mediated EphA2 degradation triggers disruption of the blood-brain barrier during Streptococcus suis meningitis

Fig. 2: EphA2 deficiency augments S. suis-induced disruption of blood brain barrier in vitro and in vivo.

A, B Immunoblot analysis of ZO-1 and EphA2 in EphA2+/+ or EphA2−/−hCMEC/D3 cells infected with SC19 (A) or D39 (B) for 0, 2, 4 h. C, D Immunoblot analysis of ZO-1 and EphA2 in EphA2−/−hCMEC/D3 cells transfected with Flag-tagged EphA2 and infected with SC19 (C) or D39 (D) for 0, 2, 4 h. E, F The TEER value in the absence and presence of EphA2 in transwell SC19 (E) or D39 (F) infection model for indicated time. For animal experiments, EphA2+/+ (total N = 90) and EphA2−/− mice (total N = 75) were intraperitoneally inoculated with SC19 and D39 for 48 h. After infection, brains were collected for indicated assays. G, H Immunoblot analysis of ZO-1 and EphA2 (total N = 36, each group n = 3). I, J bacterial load in the blood and brain. K blood-brain barrier permeability via Evans Blue staining (total N = 75, each group n = 5). L Representative images of histopathological change of brains via H&E staining (total N = 54, each group n = 3). Data are representative of three independent experiments with triplicate samples in vitro or three or five mice per group in vivo. All data are presented as mean ± SD. P ≤ 0.05 was considered as statistical significance.

Back to article page