LPS stimulating neutrophils firmly adhered to ICAM-1 to form extracellular traps depends on integrin Mac-1 and cytoskeletal proteins.
10.7507/1001-5515.202105019
- Author:
Tiantian HONG
1
;
Wang LIU
1
;
Jiaqi HUANG
1
;
Baisong ZHAO
2
;
Ying FANG
1
;
Jianhua WU
1
;
Jiangguo LIN
3
Author Information
1. School of Biology and Biological Engineering, South China University of Technology, Guangzhou 510006, P.R.China.
2. Department of Anesthesiology, Guangzhou Women and Children's Medical Center, Guangzhou 510623, P.R.China.
3. Research Department of Medical Sciences, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510080, P.R.China.
- Publication Type:Journal Article
- Keywords:
Talin-1;
cytoskeleton;
neutrophil extracellular traps;
β2 integrin
- MeSH:
Cytoskeletal Proteins;
Endothelial Cells;
Extracellular Traps;
Integrins;
Intercellular Adhesion Molecule-1;
Lipopolysaccharides/pharmacology*;
Macrophages;
Neutrophils
- From:
Journal of Biomedical Engineering
2021;38(5):903-910
- CountryChina
- Language:Chinese
-
Abstract:
Neutrophil extracellular traps (NETs) play an important role in the formation of immunothrombosis. However, how vascular endothelial cells mediate the formation of NETs has not been fully understood. We stimulated neutrophils firmly attached on the endothelial cell surface intercellular adhesion molecule-1 (ICAM-1) with lipopolysaccharide (LPS) or phorbol-12-myristate-13-acetate (PMA) for 4 h, then labeled NETs-DNA with Sytox green dye and the formation of NETs was observed by fluorescent microscopy. The area and fluorescence intensity of NETs-DNA were analyzed to quantify the formation of NETs. The results showed that both PMA and LPS were able to induce firmly adhered neutrophils on ICAM-1 to produce NETs. NETs induced by PMA were independent of neither β2 integrin lymphocyte function-associated antigen-1 (LFA-1) nor macrophage antigen complex-1 (Mac-1). In contrast, LPS-stimulated NETs were mediated by Mac-1 integrin, but not by LFA-1. After inhibition of actin filaments or Talin-1, the formation of NETs irrespective of the stimulus was significantly reduced. This study reveals the mechanism of the direct interaction between neutrophils and endothelial cells to produce NETs under inflammatory conditions, providing a new theoretical basis for the treatment of related diseases and the development of new drugs.
