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Journal of Biochemistry Advance Access published online on September 10, 2007
Journal of Biochemistry, doi:10.1093/jb/mvm164
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© 2007 The Japanese Biochemical Society

CEL-I, an InvertebrateN-Acetylgalactosamine-Specific C-Type Lectin, Induces TNF-{alpha} and G-CSF Production by Mouse Macrophage Cell Line RAW264.7 Cells

Tomohiro Yamanish1, Yoshiko Yamamoto1, Tomomitsu Hatakeyama2, Kenichi Yamaguchi1 and Tatsuya Oda1,*

1Division of Biochemistry, Faculty of Fisheries, and 2Department of Applied Chemistry, Faculty of Engineering, Nagasaki University, 1-14 Bunkyo-machi, Nagasaki 852-8521

*To whom correspondence should be addressed: Tatsuya Oda,Fax: +81-95-819-2799, E-mail: t-oda{at}nagasaki-u.ac.jp

Received July 8, 2007; Accepted August 9, 2007


  Abstract

Our previous studies demonstrated that CEL-I, a N-acetylgalactosamine (GalNAc)-specific C-type lectin purified from the marine invertebrate Cucumaria echinata (Holothuroidea) showed potent cytotoxicity to several cell lines such as HeLa , MDCK, and XC cells. In this study, we found that CEL-I induced increased secretion of tumor necrosis factor {alpha} (TNF-{alpha}) and granulocyte colony stimulation factor (G-CSF) by mouse macrophage cell line RAW264.7 cells in a dose-dependent manner, whereas this cell line was highly resistant to CEL-I cytotoxicity. The cytokine-inducing activity of CEL-I was stronger than that of phytohemagglutinin (PHA-L). A binding study using FITC-labeled CEL-I (F-CEL-I) indicated that the amount of bound F-CEL-I on RAW264.7 cells was greater than that of F-PHA-L, suggesting that the greater activity of CEL-I to induce cytokine secretion by RAW264.7 cells is partly due to the higher binding ability. Since the cell binding and cytokine-inducing activity of CEL-I were partly but significantly inhibited by the specific sugar (GalNAc), it is considered that the binding of CEL-I to cell-surface specific saccharide moieties, which may be recognized by CEL-I with higher affinity than GalNAc, is essential for the induction of cytokine secretion. The secretion of TNF-{alpha} and G-CSF from CEL-I-treated RAW264.7 cells were almost completely prevented by brefeldin A (BFA), whereas increase in mRNA levels of these cytokines were not affected by BFA. Bio-Plex beads assay suggested that temporal increase in phosphorylation of extracellular regulated kinase (ERK), c-jun NH2-terminal kinase (JNK), and p38 MAP kinase occurred at relatively early time following CEL-I treatment. Furthermore, the secretion of TNF-{alpha} and G-CSF were inhibited by specific inhibitors for these MAP kinases. These results suggest that the intracellular signal transduction through the activation of MAP kinase system is involved in CEL-I-induced cytokine secretion.

Key Words: C-type lectin, Cucumaria echinata, cytokines, granulocyte colony stimulating factor, macrophage cell line, tumor necrosis factor {alpha}


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