Lipopolysaccharide (LPS) increases tumor necrosis factor-alpha related apoptosis induced-ligand (TRAIL) in macrophages killing HepG2 cells.
- Author:
Lin ZHENG
1
;
Yi-da YANG
;
Guo-cai LÜ
;
Bing RUAN
;
Ji-fang SHENG
;
Ya-gang CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Carcinoma, Hepatocellular; pathology; Enzyme-Linked Immunosorbent Assay; Humans; Lipopolysaccharides; pharmacology; Liver Neoplasms; pathology; Macrophages; metabolism; TNF-Related Apoptosis-Inducing Ligand; biosynthesis; genetics; pharmacology; Tumor Cells, Cultured
- From: Chinese Journal of Hepatology 2005;13(9):689-691
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the influence of lipopolysaccharide (LPS) on macrophages expressing TNF-alpha related apoptosis induced-ligand (TRAIL) and its relation to apoptosis of HepG2 cell line.
METHODSMembrane-bound TRAIL (mTRAIL) was measured by flow cytometry; soluble TRAIL in supernatant was detected by enzyme-linked immunoabsorbent sandwich assay (ELISA); cytotoxicity of TRAIL to HepG2 cell line was measured by chromium release assay, and apoptosis of HepG2 cell was confirmed by Annexin V staining.
RESULTSLPS only slightly increased membrane-bound TRAIL expression of macrophages. On the other hand, soluble TRAIL in the supernatant was increased with LPS stimulation, and the optimal concentration of LPS was 100 ng/ml (sTRAIL value 67.40 ng/ml+/-5.08 ng/ml). The soluble TRAIL in the supernatant was cytotoxic to HepG2 cells, and this activity can be blocked by TRAIL neutralizing antibodies.
CONCLUSIONLPS increases the expression of soluble TRAIL in macrophages, and soluble TRAIL is toxic to HepG2 cells. All of our results indicate that TRAIL may play an important role in the pathogenesis of viral hepatitis.
