Fig. 5

CXCR3 signaling modulates resident retinal inflammation. A Representative images indicating treatment with the CXCR3 antagonist AMG487 reduced Müller fiber staining at 48 h following LPS-challenge (green; arrows). Corresponding quantification showed significantly reduced Müller glia activation (*p < 0.05). B Treatment with AMG487 reduced amoeboid microglia activation (Iba1; green, arrows). Corresponding quantification of amoeboid microglia showed that AMG487 treatment strongly reduced microglia activation compared to vehicle (***p < 0.0005). C AMG487 treatment reduced LPS-induced macrophage infiltration (F4-80; green, arrows), but corresponding quantification showed a trend that did not reach significance. D To confirm the microglial results staining was also performed for CD68, which showed a similarly significantly reduced presence of amoeboid cells following AMG487 treatment. E In contrast, treatment with the CXCR3 agonist VUF11222 strongly induced astrocyte and Müller glia reactivity (GFAP, arrows). Corresponding quantification showed a significant increase in relative GFAP intensity in the inner retina in the agonist treated group compared to vehicle. F VUF11222 treatment had no effect on microglial activation. G A cartoon outlining a proposed signaling pathway by which lipoxins inhibit neuroinflammatory responses. (GCL; ganglion cell layer, IPL; inner plexiform layer, INL; inner nuclear layer, bars represent 100 µm, graph bars represent SE)