Figure 3
From: IL-1α promotes liver inflammation and necrosis during blood-stage Plasmodium chabaudi malaria
IL-1α deficiency leads to transient higher parasitemia but attenuates the body weight loss, hypothermia and liver damage. C57BL/6 and Il1a−/− mice were infected with 1 × 106 P. chabaudi-iRBCs. Non-infected mice (day 0) were used as controls. (A) Parasitemia curves. (B) Body weight change. (C) Body temperature. (A–C) The data are expressed as the means ± SD (n = 5) of one representative experiment out of three. C57BL/6 (solid line) and Il1a−/− (dashed line). (D) H&E-stained liver sections showing necrotic foci (asterisk) and cellular infiltration at day 7 p.i. (5x and 20x magnification; bar scale corresponds to 300 and 50 μm, respectively). (E) Semiquantitative histopathological scores of inflammation, necrosis and total histopathology (inflammation and necrosis) at day 7 p.i. The data were pooled from three independent experiments (n = 10–11). (F) Serum ALT, AST and LDH concentrations. The data were pooled from three independent experiments (n = 3–9). (G) Immunofluorescence staining for TUNEL (green), F-actin (red) and nuclei (DAPI, blue) in the frozen liver sections (40x magnification; bar scale corresponds to 100 μm). (H) TUNEL+ cells per field in the liver sections. The data are expressed as the means ± SD (n = 3) of one representative experiment out of three. Significant differences were observed between C57BL/6 and Il1a−/− mouse groups with *p < 0.05, **p < 0.01 and ****p < 0.0001, using the Two-way ANOVA and Sidak’s multiple comparisons test (A–C) or the Mann-Whitney test (F, E and H).
