The effects of TNF alpha and IFN gamma on the expression of pattern recognition receptors on the surface of mouse alveolar macrophages.
- Author:
Hong HUANG
1
;
Jian-xin JIANG
;
Pei-fang ZHU
;
Zheng-guo WANG
;
Dao-jie ZHANG
;
Cheng YANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cells, Cultured; Interferon-gamma; pharmacology; Lipopolysaccharide Receptors; biosynthesis; genetics; Macrophages, Alveolar; metabolism; Mice; RNA, Messenger; genetics; Receptors, Pattern Recognition; biosynthesis; Toll-Like Receptor 2; biosynthesis; genetics; Toll-Like Receptor 4; biosynthesis; genetics; Toll-Like Receptor 9; biosynthesis; genetics; Tumor Necrosis Factor-alpha; pharmacology
- From: Chinese Journal of Surgery 2005;43(11):740-744
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of tumor necrosis factor alpha (TNF alpha) and interferon gamma (IFN gamma) on the expression of pattern recognition receptors (PRRs) on the surface of mouse alveolar macrophages.
METHODSAlveolar macrophages from mouse were cultured in DMEM supplemented with 10% (V/V) endotoxin-free calf serum. After the alveolar macrophages were stimulated with TNF alpha and IFN gamma (concentration, 20 ng/ml) for 3 h, 6 h and 12 h, the expression of PRRs, including cluster of differentiation 14 (CD14), scavenger receptor (SR), toll-like receptor 4 (TLR4), TLR2 and TLR9 mRNA and proteins were examined by RT-PCR and immunohistochemistry.
RESULTSThe expressions of CD14, TLR2 and TLR9 receptors, which were related with cellular activation, were up-regulated by the stimulation of TNF alpha and IFN gamma (P < 0.05), while SR, which was related with cellular defense action, was down-regulated (P < 0.05). Although the expression of TLR4 was up-regulated, there was no statistical significance (P > 0.05).
CONCLUSIONSThe cytokines such as TNF alpha and IFN gamma could also produce feedback regulation on the expression of PRRs at the levels of genes and proteins. Such regulation on the PRRs expression would be significant for further amplification of inflammation cascade and eventually leading to uncontrolled inflammation.