Bactericidal permeability increasing protein inhibits lipopolysaccharide-mediated platelet activation in vitro.
- Author:
Xian-Ming LUO
1
;
Qiu-Hong YANG
;
Jing WEI
;
Li-Ping MA
Author Information
1. Department of Hematology, Sun Yat-Sen University, Guangdong Province, China.
- Publication Type:Journal Article
- MeSH:
Antimicrobial Cationic Peptides;
pharmacology;
Blood Proteins;
pharmacology;
Humans;
Inflammation;
Lipopolysaccharides;
adverse effects;
Platelet Activation;
drug effects;
Platelet-Rich Plasma;
metabolism;
Toll-Like Receptor 4;
metabolism
- From:
Journal of Experimental Hematology
2012;20(1):129-132
- CountryChina
- Language:Chinese
-
Abstract:
This study was purposed to investigate the inhibitory effect of bactericidal permeability-increasing protein (BPI) on lipopolysaccharide (LPS)-mediated activation of platelets. Venous blood samples were obtained from 10 healthy volunteers and were prepared into platelet-rich plasma (PRP, 1 × 10(8)/ml). Experiments were divided into four groups: normal platelet group (untreated group); LPS group, BPI group and BPI+LPS group. PRP were stimulated by LPS (10 µg/ml) in the presence and absence of BPI (100 µg/ml) or BPI alone. Then platelets were harvested and determined for Toll-like receptor-4 (TLR-4) with flow cytometry (FCM), the supernatant was used for detection of cytokines including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) with enzyme-linked immunosorbent assay (ELISA). The results showed that as compared with normal platelet group, TLR-4 expression on platelets was significantly increased under LPS stimulation (P < 0.001); the levels of TNF-α and IL-6 in the supernatant were also remarkably elevated (P < 0.001). However, either TLR-4 expression or the cytokine levels significantly decreased in the presence of BPI when platelets underwent LPS-challenge (P < 0.05), but still were higher than that in normal platelet group. Stimulating the platelets with BPI alone could not enhance the TLR-4 expression and cytokine levels. It is concluded that BPI has the ability to inhibit the LPS-induced platelet activation.
