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. 2013 Mar 21;8(3):e59965. doi: 10.1371/journal.pone.0059965

Figure 5. Involvement of ICAM-1 in thrombin-induced lung PMN infiltration.

Figure 5

( A ) Effect of ICAM-1 blockade on thrombin-induced lung PMN infiltration in mice. ICAM-1 mAb (1 mg/kg body weight) or rat IgG was injected i.p. 0.5 h before thrombin challenge of mice. After 2 h, lungs were isolated and analyzed for PMN infiltration by measuring MPO activity. Bars indicate mean ± SEM (n = 5–6 for each condition). ***, p<0.001 compared with unchallenged control; ##, p<0.01 compared with thrombin-challenged control or thrombin-challenged IgG control. ( B ) Effect of ML-7 on thrombin-induced ICAM-1 expression in the lungs of mice. ML-7 (2.5 mg/kg) was injected i.p. 0.5 h before thrombin challenge of mice. After 2 h, lungs were isolated and analyzed for ICAM-1 expression by immunoblotting. Cu-Zn SOD levels were used to monitor loading. ( C ) The bar graph represents the effect of ML-7 on thrombin-induced ICAM-1 expression in ( B ). ICAM-1 protein expression normalized to Cu-Zn SOD level is expressed as ICAM-1/Cu-Zn SOD ratio. Data are mean ± SEM (n = 3–5 for each condition). **, p<0.01 compared with unchallenged control; ##, p<0.001 compared with thrombin-challenged control. ( D ) The bar graph represents the effect of nmMLCK deficiency on ICAM-1 expression in lungs of mice challenged with thrombin. WT and nmMLCK−/− mice (KO) mice were injected i.p. with thrombin. After 2 h, lungs were isolated and analyzed for ICAM-1 expression by immunoblotting. Actin levels were used to monitor loading. ICAM-1 protein expression normalized to actin level is expressed as ICAM-1/Actin ratio. Data are mean ± SEM (n = 3 for each condition). #, p<0.05 compared with thrombin-challenged WT control.