Taken together, these experiments, together with the LPS treatment experiment (Figure 5A–C), show that (1) LPS stimulation of TLR4 signaling plays a central role in the response of the leptomeningeal vasculature to infection (CLDN5 and PECAM1 redistribution, vessel swelling, and leakage), and (2) this vascular response is largely independent of leptomeningeal macrophages, by far the most abundant immune cells in the leptomeninges. Here, PECAM1 is linked to infection.