Fig. 2From: IL-33 deficiency causes persistent inflammation and severe neurodegeneration in retinal detachmentRD results in an acute inflammatory response in WT retina. At different days following RD, the retinas were collected and processed for RT-PCR analysis of inflammatory genes in WT mice (a–f). The mRNA expression of CCL2 (a), C1ra (b), C1s (c), IL-1β (d) and IL-18 (e) at days 1, 4, 7, and 28 post-RD. f The expression level of TNFα peaked at day 4 and remained at the peak at day 7 and returned back to the basal level at day 28 post-RD. g The expression level of IL-33 peaked at day 1, then decreased towards the basal level at day 28 post-RD. h The expression level of GFAP peaked at day 1 and reduced gradually. At day 28 post-RD, the expression level of GFAP was maintained at a higher level than control. Data presented as mean ± SEM, n = 6 per group, one-way ANOVA followed by Dunnett’s multiple comparisons test, *P < 0.05, **P < 0.01, ***P < 0.001. i, j Representative images of retinal sections stained for glutamine synthetase (red, marker for Müller cells), IL-33 (green) and DAPI (blue) in i detached retina (day 28 post-RD) and j normal retina. IL-33 was localised in the nuclei of Müller cells, and no significant IL-33 signal (green) could be observed out of Müller cells in detached retina. Scale bar, 50 μmBack to article page