Fig 1: ICAM1 is upregulated in brain endothelial cells and LFA1 is elevated in brain tissue T cells collected from MPTP-treated mice. (A) Representative images of ICAM1 in brain tissue endothelial cells of saline- or MPTP- treated mice. MPTP-treated mice exhibited increased levels of ICAM1. (B) Endothelial cells collected from the brains of MPTP-treated mice expressed significantly higher levels of ICAM1 4 days after MPTP injection (n=9). Experiments were performed in triplicate. ****P<0.0001. (C) Representative images of LFA1 expressed in different tissues of MPTP-treated mice. Brain tissue exhibited higher expressions of LFA1 on T cells. T cells (CD45+CD3+) were collected from the blood, spleen and brain of MPTP-treated mice. (D) T cells in the brain of MPTP-treated mice expressed significantly increased levels of LFA1 compared with the blood and spleen at day 4 after MPTP injection. n=9. Experiments were performed in triplicate. *P<0.05 and ***P<0.001. ICAM1, intercellular adhesion molecule 1; LFA1, lymphocyte function-associated antigen-1; MPTP, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.
Fig 2: Blocking of ICAM1 or CD11a attenuates the severity of MPTP-induced PD in mice. (A) Blocking of ICAM1 or CD11a increased the levels of TH+ cells at day 4 after MPTP injection. Mouse behaviour assessed by open field tests showed improved clinical presentation in those treated with ICAM1 or CD11a blockade at day 4 after MPTP injection, including (B) distance moved, (C) rears and (D) grooms. n=9. Experiments were performed in triplicate. **P<0.01 and ***P<0.001. ICAM1, intercellular adhesion molecule 1; MPTP, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; TH, tyrosine hydroxylase; CTRL, control; α-ICAM1, anti-ICAM1 antibodies; α-CD11a, anti-CD11a antibodies.
Fig 3: Nilotinib inhibits cell adhesion and monocyte activation. (A) PCA plot of log 2-transformed LFQ intensities from THP-1 cells pre-treated with DMSO, 5 μM nilotinib, or imatinib for 1 h before stimulation with live E. coli for up to 24 h, showing distinct grouping of treatments. (B,C) Volcano plot of THP-1 cells treated with (B) nilotinib vs imatinib and (C) nilotinib vsE. coli, a cutoff of FDR <0.05, and a 1.5-fold change between conditions. (D) Expression levels of CD44, (E) CD11c, (F) CD14, (G) CD49a, and (H) CD54 on the cell surface were measured by flow cytometry. (I) Optical density of dissolved crystal violet was used to evaluate the adhesion rate. Significant differences between two groups were determined by the Mann–Whitney U-test. The statistical significance of the comparisons with E. coli is indicated as follows: ns, not significant; *, P ≤ 0.05; **, P ≤ 0.01. Error bars represent the standard deviation of four biological replicates.
Supplier Page from Thermo Fisher Scientific for CD54 (ICAM-1) Antibody FITC