Skip to main content
. Author manuscript; available in PMC: 2019 Mar 1.
Published in final edited form as: Cell Microbiol. 2018 Jan 18;20(3):10.1111/cmi.12811. doi: 10.1111/cmi.12811

Fig 3. Blocking EphA2 activity diminishes the crossing of C. neoformans.

Fig 3

(A) Addition of peptide monoclonal antibody (mAb) against the extracellular N-terminal region of EphA2 blocks activity of EphA2. Brain endothelial cells were treated with EphA2-mAb (125μg) for 45mins and subsequently challenged with C. neoformans. Following a 3h co-incubation in the in vitro BBB model, transcytosis assays showed reduced fungal crossing, in contrast to the control antibody (IgG). (B) Treatment of endothelial cells with the antibodies did not affect dextran permeability suggesting an intact barrier. (C) & (D) Similarly, addition of 10μm or 20μm dasatinib (an inhibitor of EphA2) to brain endothelial cells in the in vitro BBB model, reduced fungal crossing but did not appear to alter dextran permeability. The DMSO solvent control had no effect on fungal crossing. Transcytosis assays were performed as described above. n=8, *P<0.05, ***P<0.001, n/s = not significant.