Biomedical Science Letters (대한의생명과학회지)

The Korean Society for Biomedical Laboratory Sciences (대한의생명과학회)
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Chemotactic Effect of Leukotactin-1/CCL15 on Human Neutrophils

  • Lee Ji-Sook (Department of Clinical Laboratory Science, School of Medicine, Eulji University, Department of Biology, College of Natural Sciences, Daejeon University) ;
  • Yang Eun-Ju (Department of Clinical Laboratory Science, School of Medicine, Eulji University, Department of Biomedical Laboratory Science, College of Health Science, Yonsei University) ;
  • Ryang Yong-Suk (Department of Biomedical Laboratory Science, College of Health Science, Yonsei University) ;
  • Kim In-Sik (Department of Clinical Laboratory Science, School of Medicine, Eulji University)
  • Published : 2006.09.01
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Abstract

Leukotactin-l (Lkn-l )/CCL15 has been known as a potent chemoattractant of leukocytes. However, the precise function of Lkn-l in human neutrophils has not been explained well. In the present study, we investigated the contribution of Lkn-1 in chemotactic activity of human neutrophils. Both CCR1 and CCR3 mRNA expressions are strongly expressed in human neutrophils but CCR2 protein expression was uniquely detected on the cell surface. Lkn-l binding to CCR1 and CCR3 induced chemotactic activity of neutrophils. Chemotactic index of Lkn-l was comparable to that of IL-8. $MIP-1{\alpha}/CCL3$ binding to CCR1 and CCR5 has no effect on neutrophil migration. Cell migration, in response to Lkn-l, was blocked by pertussis toxin (Ptx), a $G_o/G_i$ protein inhibitor, and U73122, a phospholipase C(PLC) inhibitor but not by protein kinase C inhibitor such as rottlerin, and Ro-31-8425. Taken together, our results demonstrate that Lkn-l transduces the chemotaxis signal through $G_o/G_i$ protein and PLC. This finding provides the molecular mechanism by which Lkn-l may contribute to neutrophil movement into the site of inflammation.

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