Involvement of nuclear factor-κB in lipoteichoic acid-induced cyclooxygenase-2 expression in RAW 264.7 macrophages

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Abstract
We have investigated the role of protein kinase C (PKC) and nuclear factor‐κB (NF‐κB) in cyclooxygenase‐2 (COX‐2) expression caused by Staphylococcus aureus lipoteichoic acid in RAW 264.7 macrophages. A phosphatidylcholine‐phospholipase C (PC‐PLQ inhibitor (D‐609) and a phosphatidyl‐inositol‐phospholipase C (Pl‐PLC) inhibitor (U‐73122) attenuated lipoteichoic acid‐induced COX‐2 expression, while a phosphatidate phosphohydrolase inhibitor (propranolol) had no effect. Two PKC inhibitors (Go 6976 and Ro 31–8220) and the NF‐κB inhibitor, pyrrolidine dithiocarbamate (PDTC), also attenuated lipoteichoic acid‐induced COX‐2 expression. Lipoteichoic acid resulted in a decrease in PKC activity in the cytosol and an increase in PKC activity in membranes. The lipoteichoic acid‐induced translocation of p65 NF‐κB from the cytosol to the nucleus was inhibited by D‐609, U‐73122, Go 6976, Ro 31–8220, and PDTC., but not by propranolol. The results suggested that lipoteichoic acid might have activated PC‐PLC and Pl‐PLC to induce PKC activation, which in turn initiated NF‐κB activation, and finally induced COX‐2 expression in RAW 264.7 macrophages.