Caffeic acid phenethyl ester suppresses the induction of eotaxin in human lung fibroblast cells.

BACKGROUND: Eotaxin, a CC chemokine, plays an important role in inflammation of airway allergic diseases. The authors investigated the activities of caffeic acid phenethyl ester (CAPE), the active component of propolis, in regulating eotaxin production in human lung fibroblast. MATERIAL AND METHODS: The authors used human lung fibroblasts, CCD-11Lu cells, stimulated with interleukin-13 (IL-13) and tumor necrosis factor-alpha (TNF-alpha), to induce eotaxin secretion. The cells were treated with CAPE of different concentrations and pretreatment duration to check its inhibition in eotaxin production. Enzyme-linked immunosorbent assay (ELISA) was used to measure eotaxin secretion; electrophoretic mobility shift assay (EMSA) to check nuclear factor kappa B (NF-kappaB)-promoter binding; and Western blot to quantitate the cyplasmic inhibitor of NF-kappaB (IkappaB) and nuclear NF-kappaB p65. RESULTS: CAPE inhibited the production of eotaxin in CCD-11Lu cells stimulated by IL-13 and TNF-alpha combination in a dose- and time-dependent manner. The authors also demonstrated CAPE to be able to inhibit NF-kappaB activation in CCD-11Lu cells. CONCLUSION: The authors suggest that CAPE is a promising agent in controlling eosinophils influx in human airway.

Soluble CD26/30 levels before and after treatment with interferon-alpha and ribavirin combination therapy in a pediatric hepatitis C patient.

Chronic hepatitis C virus (HCV) infection frequently leads to end-stage liver diseases and extrahepatic complications. Combination therapy with interferon-alpha (IFN-alpha) and ribavirin is now recommended as the first-line therapy for patients with chronic hepatitis C in adults. However, the benefit of such combination therapy in children with hepatitis C is still under investigation. We report here on a 6-year-old boy admitted with chronic active hepatitis C infection and treated with interferon-alpha and ribavirin. After treatment for 12 months, his serum showed negative HCV RNA, and normal alanine aminotransferase, and there was a sustained response. The patient's serum soluble CD30 (sCD30) level was higher than that of controls (>100 U/mL vs 46 +/- 11 U/mL) before combination therapy but there was no difference in soluble CD26 (sCD26) [103 ng/mL vs 119 +/- 28 ng/mL]. The sCD30 decreased and sCD26 increased at 6 months (45 U/mL and 188.3 ng/mL, respectively) using combined therapy as well as at 4 months after discontinuing it (33 U/mL and 167.8 ng/mL, respectively) in our patient. The results indicate that combined treatment with IFN-alpha and ribavirin may be used as the first-line treatment for children with chronic hepatitis C. The changes of sCD30 and sCD26 may be helpful in estimating of HCV infection activity.