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Innate Immunity
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Role of actin cytoskeleton in LPS-induced NF-{kappa}B activation and nitric oxide production in murine macrophages

Sandeepa M. Eswarappa

Centre for Infectious Disease Research and Biosafety Laboratories, Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, Karnataka, India

Vidhi Pareek

Centre for Infectious Disease Research and Biosafety Laboratories, Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, Karnataka, India

Dipshikha Chakravortty

Centre for Infectious Disease Research and Biosafety Laboratories, Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, Karnataka, India, dipa{at}mcbl.iisc.ernet.in

Lipopolysaccharide (LPS) is a major cell wall component of Gram-negative bacteria and is known to cause actin cytoskeleton reorganization in a variety of cells including macrophages. Actin cytoskeleton dynamics influence many cell signaling pathways including the NF-{kappa}B pathway. LPS is also known to induce the expression of many pro-inflammatory genes via the NF-{kappa}B pathway. Here, we have investigated the role of actin cytoskeleton in LPS-induced NF-{kappa}B activation and signaling leading to the expression of iNOS and nitric oxide production. Using murine macrophages, we show that disruption of actin cytoskeleton by either cytochalasin D (CytD) or latrunculin B (LanB) does not affect LPS-induced NF-{kappa}B activation and the expression of iNOS, a NF-{kappa}B target gene. However, disruption of actin cytoskeleton caused significant reduction in LPS-induced nitric oxide production indicating a role of actin cytoskeleton in the post-translational regulation of iNOS.

Key Words: Actin • cytochalasin D • iNOS • latrunculin B • lipopolysaccharide • NF-{kappa}B

Innate Immunity, Vol. 14, No. 5, 309-318 (2008)
DOI: 10.1177/1753425908096856
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