Depolymerization of Actin Filament by Cytochalasin E Induces Interleukin-8 Production and Up-Regulates CD54 in the HeLa Epithelial Cell Line

Abstract

We previously reported that the depolymerization of actin filament by cytochalasin E enhances low affinity Fcε receptor II (CD23) expression on the human monocyte-like cell line, U937 (J. Clin. Immunol. 20: 235, 2000). In this study, we found that cytochalasin E strongly induces interleukin-8 through an epithelial cell line, HeLa, in dose- and time-dependent manners as assessed by enzyme-linked immunoassay and reverse transcription-polymerase chain reaction techniques. In addition, interleukin-8 production in the HeLa cells cultured with cytochalasin E was blocked in the presence of protein kinase C inhibitors, Go6976 and H-7. On the other hand, it was found that CD54 (intercellular adhesion molecule-1; ICAM-1) expression on the HeLa cells and the secretion of soluble CD54 were significantly up-regulated after culturing with cytochalasin E, and that these up-regulations of CD54 were also suppressed by Go6976. Taken together, these findings indicate that cytochalasin E activates protein kinase C under the depolymerization of actin filament, leading to the induction of interleukin-8 production and the up-regulation of CD54 in HeLa cells.