Fig. 3.

Roles of histone H4 and TLRs in Cl₂ induced inflammatory lung injury. Twenty four hours after Cl₂ exposure (400 ppm, 30 min) in WT, Tlr2-KO, and Tlr4-KO mice, PaO₂ (3A) and lung wet/dry mass ratio (3B) were measured. Pulmonary endothelial activation was represented by P-selectin expression (3C) (Scale bars: 100 μm) and circulating vWF (3D). Pulmonary neutrophil infiltration was shown by Ly6G marker staining (3E) (Scale bars: 50 μm), and neutrophilic activation was indicated by MPO activity (3F). The protein levels of inflammatory cytokines TNF-α (3G) and IL-1β (3H) were measured by western blot. Histone H4 (10 mg/kg) or anti-H4 antibody (20 mg/kg) was delivered through the tail vein 1 h prior to Cl₂ exposure. N = 6 independent replicates for all groups. *p < 0.05, **p < 0.01 compared with the control group; ^#p < 0.05, ^##p < 0.01 compared with the WT mice treated solely with Cl₂; ^$p < 0.05, ^$$p < 0.01 compared with the WT mice treated in the same manner (Cl₂ + H4); ^&p < 0.05, ^&&p < 0.01 compared with the WT mice treated in the same manner (Cl₂ + Anti-H4).