Fig. 2

Inactivation of ANXA2 impeded rickettsial attachment to the endothelial cells in vitro. Extracellular adhesive bacteria in anti-ANXA2 (AntiA2)-treated HUVECs at 0.1 (n = 5), 1 (n = 10), and 3 (n = 5) µg/ml (a) or BMECs from WT (n = 6) and Anxa2-null (n = 6) mice (b) were enumerated by IF microscopy at 15 min p.i. with R. australis at 10 MOI. Normal mouse IgG was used as control IgG (Ctl IgG, 3 µg/ml) (n = 5). All ECs were fixed with 4% paraformaldehyde as impermeable fixation. Data are represented as mean ± SEM. **compared to the control group, P < 0.01