Figure 1
From: Apoptosis inhibitor of macrophage ameliorates fungus-induced peritoneal injury model in mice
Morphological changes in the zymosan-induced peritonitis model. (a) Strong inflammatory cell infiltration associated with a necrotic area was demonstrated up to 4 weeks in AIM-deficient mice; in contrast, these changes subsided at 3 weeks after disease induction in the wild mice. The first and second rows: AIM +/+ mice, The third and fourth rows: AIM −/− mice; The second and fourth rows show higher magnifications of the images in the boxed areas of the first and third rows, respectively. HE stain, arrows: necrotic area, Scale bars, 200 μm. Sham and Day 7–21: n = 6, Day 28: n = 14. (b) Light microscopic findings indicated necrosis associated with strong neutrophilic infiltration with karyorrhexis. The figures are enlarged views of day 14 in Fig. 1a. The left two photographs present the findings in AIM +/+ mice, and the right two in AIM −/− mice. The insets in the large magnified photos indicate karyorrhexis. Karyorrhexis is a degenerative cellular process characterized by fragmentation of the condensed nucleus and irregular distribution of the resultant chromatin in the cytoplasm47. HE stain, Scale bars, 200 μm (each left figure) and 20 μm (each right figure). (c) Expression of F4/80 positive macrophages in the zymosan-induced peritonitis model. Macrophage infiltration continued up to 4 weeks in AIM-deficient mice, while it decreased 3 weeks after disease induction in the wild mice. Left figures: The second and fourth rows show higher magnifications of the images in the boxed areas in the corresponding images in the first and third rows, respectively. Right graphs: Macrophage positive areas were assessed by morphometry and were expressed as ×103 μm2/mm surface length. W: AIM +/+ mice; K: AIM −/− mice; CTL: control normal AIM +/+ mice, Scale bars, 200 μm. n = 6 for each group.
