Krüppel-Like Factor 5 Mediates Proinflammatory Cytokine Expression in Lipopolysaccharide-Induced Acute Lung Injury through Upregulation of Nuclear Factor-<b><i>κ</i></b>B Phosphorylation <i>In Vitro</i> and <i>In Vivo</i>

<table>Effects of lipopolysaccharide (LPS) exposure on Krüppel-like factor 5 (KLF5) and nuclear factor-kappaB subunit protein expression in human bronchial epithelial cells. Cells from the (a) HBEC and (b) BEAS-2B lines were incubated with LPS (5 <i>μ</i>g/mL) for various durations, and KLF5, p65, phospho-p65 (Ser276), and phospho-p65 (Ser536) protein expression were evaluated using western blotting. The time to peak intensities of KLF5, p65, Ser276, and Ser536 phosphorylation differed slightly. Data were obtained from 3 independent experiments.</table>

Mediators of Inflammation

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Figure 2

Figure 2: Krüppel-Like Factor 5 Mediates Proinflammatory Cytokine Expression in Lipopolysaccharide-Induced Acute Lung Injury through Upregulation of Nuclear Factor-<b><i>κ</i></b>B Phosphorylation <i>In Vitro</i> and <i>In Vivo</i> 

Figure 2 | Krüppel-Like Factor 5 Mediates Proinflammatory Cytokine Expression in Lipopolysaccharide-Induced Acute Lung Injury through Upregulation of Nuclear Factor-κB Phosphorylation In Vitro and In Vivo 