Fig. 3
a Photomicrographs of spleen tissue stained with hematoxylin and eosin. Original magnification × 1000; bars = 100 μm. Mice were inoculated with 5 × 106 parasitized RBCs or saline and treated with BM-MSCs. Spleens were excised 5 days after infection. Normal spleen architecture with white pulp (double black arrows). Uninfected mice treated with BM-MSCs also displayed normal spleen architecture (double black arrows). In P. berghei-infected mice, spleen damage was observed with activation of lymphocytes in white pulp, increased deposition of malaria pigment in red pulp (single white arrows), and increased number of lymphoblasts and lymphocytes in white pulp (red double arrows). b A semiquantitative, severity-based score was used to measure malaria pigment deposition, inflammation, fibrosis, and histoarchitectural damage in spleens of mice infected with P. berghei or mock-infected with saline and, 24 hours after infection, treated with BM-MSCs. Values are expressed as median (interquartile range) of six animals in each group. *Significantly different from uninfected group (p <0.05). +Significantly different from P. berghei-infected group (p <0.05). c Representative dot-plots demonstrating CD11b+ fluorescence in splenocytes. BM-MSC bone marrow-derived mesenchymal stromal cell, FSC forward scatter, Sal saline