Figure 3
From: Toll-like receptor 2 deficiency leads to delayed exacerbation of ischemic injury
Decreased levels of MCP-1 and CD45 high /CD11b + expressing cells in Toll-like receptor 2 deficient mice. (A-C) Expression analysis of inflammatory cytokines IL-1β, IL-6 and TNF-α on protein levels 1 and 4 days after transient middle cerebral artery occlusion (MCAO) revealed no significant difference between wild-type (WT) and Toll-like receptor (TLR) 2−/− groups. (D) Significant reduction of MCP-1 levels in the TLR2−/− group compared with their WT controls 1 day after transient MCAO. (E) Topographic representation of isolated brain mononuclear cells from ischemic hemispheres of control, WT and TLR2−/− mice 3 and 7 days after stroke, analyzed using two-color flow cytometry. Cells were analyzed for CD45 and CD11b, thus allowing us to distinguish two different cell populations: CD45high/CD11b+ (that is, the macrophage-like) population (red); and CD45low/CD11b+ (microglial) population (green). (F) Flow cytometric analysis showed a significant decrease in the number of CD45high/CD11b+ cells in TLR2−/− mice compared with WT mice at both 3 and 7 days after stroke. (G) Quantitative analysis of CD45low/CD11b+ cells (microglia) indicates a significant reduction in cell numbers in TLR2−/− mice as compared with WT 7 days after stroke, while 3 days after stroke the difference is not significant, but there is a tendency toward reduced cell numbers in TLR2−/− mice. Values (A-D) are expressed as mean ± SEM (n = 4, *P <0.05). Data (F, G) are expressed as percentage of CD45+ events ± SEM (n = 4; *P <0.05).