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Am J Physiol Lung Cell Mol Physiol 280: L762-L770, 2001;
1040-0605/01 $5.00
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Vol. 280, Issue 4, L762-L770, April 2001

Role of LPS-induced microfilament depolymerization in MIP-2 production from rat pneumocytes

Noritaka Isowa1 and Mingyao Liu1,2

1 Thoracic Surgery Research Laboratory, Division of Cellular and Molecular Biology, Toronto General Hospital Research Institute, University Health Network, and 2 Department of Surgery, University of Toronto, Toronto, Ontario, Canada M5G 2C4

We have previously demonstrated that lipopolysaccharide (LPS) induces production of macrophage inflammatory protein-2 (MIP-2), a C-X-C chemokine for neutrophil recruitment and activation, in primary cultured rat lung alveolar epithelial cells. We have also demonstrated that LPS depolymerizes microfilaments in rat alveolar epithelial cells. To determine whether the polymerization status of microfilaments affects LPS-induced MIP-2 production, we treated rat alveolar epithelial cells with cytochalasin D (CytoD), a microfilament-disrupting agent, before and during LPS stimulation. A lower concentration (0.1 µM) of CytoD inhibited LPS-induced MIP-2 production without affecting microfilament polymerization. In contrast, LPS-induced MIP-2 production was enhanced by a higher concentration (10 µM) of CytoD, which disrupted the filamentous structure of actin. Jasplakinolide (1 nM to 1 µM), a polymerizing agent for microfilaments, decreased LPS-induced MIP-2 secretion. Jasplakinolide (1 µM) also blocked LPS-induced depolymerization of microfilaments. These results suggest that, in alveolar epithelial cells, LPS-induced MIP-2 production is at least partially regulated by microfilament depolymerization.

cytokines; chemokines; lipopolysaccharide; macrophage inflammatory protein-2


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