Fig. 6.

Effect of histone deacetylase 6 (HDAC6) inhibition on lung myeloid differentiation primary response 88 (MyD88) acetylation, MyD88-TNF receptor-associated factor 6 (TRAF6) assembly, NF-κB acetylation, and vascular permeability after lipopolysaccharide (LPS). A: lung homogenates from mice obtained 3 h after LPS (2 mg/kg ip) and HDAC6-I treatments (1 mg/kg ip) were used to immunoprecipitate MyD88. TRAF6, acetylated lysine, and MyD88 were probed in MyD88 immunoprecipitates by immunoblotting, with densitometry shown (B); (n ≥ 5/group). C: acetylated p65 was quantified in lung homogenates of 7-day-old mouse pups 6 h after LPS and HDAC6-I treatments by immunoblotting, with densitometry quantification shown (D). E, F, and G: bronchoalveolar lavage (BAL) fluid from control and LPS-, LPS + HDAC6-I-, and LPS + pan-HDAC-I-treated mice obtained at 24 h was used to quantify the total number of cells (E), protein concentration (F), and macrophage, lymphocyte, and polymorphonuclear leukocyte (PMN) counts (G); (n ≥ 5/group). Capped lines, with significance level (***P < 0.001), denote significant comparison of groups (B, D, and F) using ANOVA and post hoc Tukey test.