Additional file 1 of Lipoxins A4 and B4 inhibit glial cell activation via CXCR3 signaling in acute retinal neuroinflammation

Additional file 1: Table S1. Antibodies Used. Figure S1. High magnification images of cell marker staining. A) Representative retinal staining at 1 day following intravitreal LPS challenge, shown at higher magnification to better demonstrate cell morphology of GFAP, F4-80, and GR-1. B) Representative retinal staining for ramified or amoeboid microglial morphology following staining for Iba1 or CD68. (scale bars represent 20 μm). Figure S2. LPS challenge did not induce an apparent T-cell response. Representative negative staining for CD4- and CD3-positive T cells in retinal sections at three days following intravitreal LPS treatment showed no signal in the retina. A parallel stained section from a retina three days after exposure to the potent oxidative stressor paraquat (PQ) is presented as a positive control (arrows, scale bars represent 100 μm). Figure S3. LPS treatment results in significant RGC loss after three weeks. A) Brn3a staining in retinas over a time course showed no clear reduction in RGC density compared to control until a 21 day time point (d21) after LPS injection (scale bars represent 100 μm). B) Corresponding quantification after 21 days reveals a small, but significant loss of RGCs at three weeks following LPS-induced retinal inflammation (*p <0.05, bars represent SE, GCL; ganglion cell layer). Figure S4. LXA4, LXB4 or Amg487 treatment alone do not induce retinal inflammation markers. Retinal staining for A)GFAP, B) Iba1, or C) F4-80, do not show any difference at two days following treatment, compared to vehicle alone (scale bars represent 100 μm).