Complement C5a‐triggered differentiated HL‐60 stimulates migration of THP‐1 monocytic leukocytes via secretion of CCL2

FEBS Open Bio

Michiyo Deushi¹  Masayuki Yoshida¹  Syed Masudur Rahman Dewan¹  Mizuko Osaka² 

[1] Department of Life Sciences and Bioethics, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Japan;Department of Life Sciences and Bioethics, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Japan;Department of Nutrition in Cardiovascular Disease, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Japan;

关键词: C5a;    CCL2;    chemotaxis;    neutrophil‐like dHL‐60;    monocytic leukocyte THP‐1;    NF‐κB p65;   

DOI  :  10.1002/2211-5463.13144

来源: Wiley

【 摘 要 】

Leukocytes play an important role in vascular inflammation prior to atherosclerosis. In particular, monocyte adhesion and migration to the endothelium contribute to the development of vascular inflammation. Previously, we showed the importance of neutrophils and complement C5a in the early phase of vascular inflammation in mice fed a high‐fat diet. However, the relationship between monocytes and neutrophils is not well understood. In this study, we elucidated the involvement of neutrophils in the migration of monocytes. We observed that C5a induces CCL2 expression in neutrophil‐like dHL‐60 cells. To investigate the physiological significance of CCL2 secretion, we performed a chemotaxis assay. Interestingly, dHL‐60 culture supernatant in the presence of C5a enhanced the migration of THP‐1 in comparison with the absence of C5a. Furthermore, CCL2 expression and secretion significantly increased in C5a‐stimulated dHL‐60 through the phosphorylation of NF‐κB p65. Actin polymerization on THP‐1 was enhanced by the presence of C5a compared with the absence of C5a when stimulated by a dHL‐60‐cultured medium. These results suggest that crosstalk between neutrophils and monocytes via CCL2 may play an important role in vascular inflammation.

【 授权许可】

CC BY