1 Tumor necrosis factor (TNF)-a is known to induce the expression of CCL11 and CCR3 via the activation of NF-kB. CCL11 (eotaxin), the C-C chemokine, is a potent chemoattractant for eosinophils and Th2 lymphocytes, and CCR3 is the receptor for CCL11. 2 In order to determine the effects of rosmarinic acid on the TNF-a-induced upregulation of CCL11 and CCR3 in human dermal fibroblasts, we performed an enzyme-linked immunosorbent assay for CCL11 and a Western blot assay for CCR3. The TNF-a-induced expression of CCL11 and CCR3 genes was attenuated by rosmarinic acid. 3 In our NF-kB luciferase reporter system, TNF-a-induced NF-kB activation was observed to be reduced by rosmarinic acid. In accordance with this result, rosmarinic acid also inhibited TNF-ainduced phosphorylation and degradation of IkB-a, as well as nuclear translocation of NF-kB heterodimer induced by TNF-a. This suggests that rosmarinic acid downregulates the expression of CCL11 and CCR3 via the inhibition of NF-kB activation signaling. 4 Using the NF-kB luciferase reporter system, Western blot analysis, and IKK-b activity assay, we determined that rosmarinic acid inhibits IKK-b activity in NF-kB signaling, which upregulates the expression of CCL11 and CCR3. Additionally, TNF-a-induced secretion of soluble intercellular adhesion molecule-1 and soluble vascular cell adhesion molecule-1 molecules was found to be attenuated by rosmarinic acid. 5 Our results show that rosmarinic acid inhibits the expression of CCL11 and CCR3 by suppressing the IKK-b activity in NF-kB activation signaling. Further, these results suggest that rosmarinic acid might inhibit the expression of NF-kB promoter-related genes.