Figure 2

Effect of genetic deletion of MLCK on intestinal permeability 6, 12, 24 and 48 h after CLP. Basal permeability to FD-4 was similar in unmanipulated (UM) MLCK^−/− and WT mice (n = 5–6/group, p = 0.2). Sepsis worsened intestinal permeability 6, 12 and 24 h after sepsis, which returned to basal levels 48 h after CLP. In contrast, permeability remained at basal levels in MLCK^−/− mice following CLP. Intestinal permeability was statistically lower in MLCK^−/− mice than WT mice at all time points where sepsis induced intestinal hyperperme-ability (n = 7–9/group at 6 h, n = 14–16/group at 12 h, n = 11–14/group at 24 h, n = 7–10/group at 48 h; p = 0.02, p = 0.0009, p = 0.02, p = 0.18 when comparing MLCK^−/− and WT mice at 6, 12, 24 and 48 h).