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-κB pathway. LPS is also known to induce the expression of many pro-inflammatory genes via the NF-κB pathway. Here, we have investigated the role of actin cytoskeleton in LPS-induced NF-κB 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-κB activation and the expression of iNOS, a NF-κB 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. © SAGE Publications 2008.
CITATION STYLE
Eswarappa, S. M., Pareek, V., & Chakravortty, D. (2008). Role of actin cytoskeleton in LPS-induced NF-κB activation and nitric oxide production in murine macrophages. Innate Immunity, 14(5), 309–318. https://doi.org/10.1177/1753425908096856
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