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  • Title: LPS-induced depolymerization of cytoskeleton and its role in TNF-alpha production by rat pneumocytes.
    Author: Isowa N, Xavier AM, Dziak E, Opas M, McRitchie DI, Slutsky AS, Keshavjee SH, Liu M.
    Journal: Am J Physiol; 1999 Sep; 277(3):L606-15. PubMed ID: 10484469.
    Abstract:
    Lipopolysaccharide (LPS) polymerizes microfilaments and microtubules in macrophages and monocytes. Disrupting microfilaments or microtubules with cytochalasin D (CytoD) or colchicine can suppress LPS-induced tumor necrosis factor-alpha (TNF-alpha) gene expression and protein production from these cells. We have recently demonstrated that primary cultured rat alveolar epithelial cells can produce TNF-alpha on LPS stimulation. In the present study, we found that the LPS-induced increase in TNF-alpha mRNA level and protein production in alveolar epithelial cells was not inhibited by CytoD or colchicine (1 nM to 10 microM). In fact, LPS-induced TNF-alpha production was further enhanced by CytoD (1-10 microM) and inhibited by jasplakinolide, a polymerizing agent for microfilaments. Immunofluorescent staining and confocal microscopy showed that LPS (10 microg/ml) depolymerized microfilaments and microtubules within 15 min, which was prolonged until 24 h for microfilaments. These results suggest that the effects of LPS on the cytoskeleton and the role of the cytoskeleton in mediating TNF-alpha production in alveolar epithelial cells are opposite to those in immune cells. This disparity may reflect the different roles between nonimmune and immune cells in host defense.
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