Heterogeneous patterns of endothelial NF-κB p65 and MAPK c-Jun activation, adhesion molecule expression, and leukocyte recruitment in lung microvasculature of mice with sepsis.

Figure S1: Overview of p65 and c-Jun nuclear localization in pulmonary microvascular beds of control and sham mice. (A) Immunohistochemical staining of p65 showed nuclear localization in arterioles (A), alveolar tissue (AT), and postcapillary venules (V) of the lung in control, sham, and mice subjected to CLP for 72 hours. Black arrows point at the red p65 positive nuclei. (B) Immunohistochemical staining for c-Jun showed nuclear localization in arterioles, alveolar tissue, and postcapillary venules of the lung in control, sham, and mice subjected to CLP for 72 hours. Black arrows point at the red c-Jun positive nuclei. Images are representative of five mice per group.

Figure S2: Distribution of macrophages in pulmonary microvascular beds of mice during CLP-induced sepsis initiation and progression. (A) The kinetics of Cd68 mRNA levels in the lung of control (C, blue, n=8), sham (green, n=10), and CLP-septic (red, n=13) mice were detected by RT-qPCR. Graphs showed individual values and mean± SD. (B) Immunohistochemical staining of CD68-positive macrophages was performed to detect their location in the lung of control, sham, and CLP-septic mice at indicated time points. Black arrows point at macrophages. Arterioles: ‘A’, alveolar tissue ‘AT’, and postcapillary venules: ‘V’. Images are representative of 8~13 mice per group.