Fig. 5

Anti-TNF antibody treatment prevents astrocyte activation and mortality in IL-10 KO mice with malaria. Mice were infected with P. chabaudi and followed throughout the acute phase of infection (day 12 p.i.) or sacrificed 8 days post-infection for immunofluorescent staining. One group of IL-10 KO mice received anti-TNF IgG treatment (n = 5), while another group of IL-10 KO mice (n = 5) and a group of WT mice received isotype IgG as control (n = 5). a Representative confocal images (× 20) of cryosections stained for astrocytes (GFAP; green) and fibrinogen (red) with DAPI (blue) in sagittal brain sections in anti-TNF antibody-treated IL-10 KO mice, b isotype IgG-treated IL-10 KO mice, c and isotype IgG-treated WT mice. d Brain fibrinogen and e GFAP staining for reactive astrocytes in the hippocampus were quantified by calculating the percent area per field of immunostaining above signal threshold. Ten fields per animal were assessed, with the graph showing the mean value per animal. f General behavior as measured by the abbreviated SHIRPA screen of anti-TNF antibody-treated (IL-10 KO, n = 5) and isotype IgG-treated (IL-10 KO, n = 5; WT, n = 5) mice infected with P. chabaudi. Green arrows represent the dosing schedule of either anti-TNF IgG or isotype control IgG. g Liver fibrinogen quantitation. Data shown is representative of two independent experiments (n = 9 total mice/group). One-way ANOVA, followed by post hoc Bonferroni method, was used to determine statistical significance. *p < 0.05, **p < 0.01, ***p < 0.001. Scale bars represent 50 μm