Study on the relationship between heat shock protein 70 and toll-like receptor-4 of monocytes.
- Author:
Xinzhong CHEN
1
;
Zongquan SUN
;
Xinling DU
;
Chao LIU
;
Yi LIU
;
Long WU
Author Information
1. Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
- Publication Type:Journal Article
- MeSH:
HSP70 Heat-Shock Proteins;
metabolism;
Humans;
In Vitro Techniques;
Monocytes;
metabolism;
Toll-Like Receptor 4;
metabolism;
Transcription Factor RelA;
metabolism;
Tumor Necrosis Factor-alpha;
metabolism
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2004;24(6):560-562
- CountryChina
- Language:English
-
Abstract:
To explore the relation between human heat shock protein 70 (hsp70) and TLR4 in human monocytes in vitro, human monocytes were stimulated with various concentrations of HSP70, and TNF-alpha production in supernatants was measured by ELISA. Pre-incubated with or without anti-TLR4 mAb, and stimulated with hsp70 (5.0 microg/ml), NF-kappaB p65 of human monocytes in different time points were detected by immunohistochemistry and monocyte surface expression of TLR4 was measured by flow cytometry. After the human monocytes were pre-incubated with various concentrations of anti-TLR4 and stimulated with hsp70 (5.0 microg/ml), TNF-alpha production in supernatants was measured. The results showed that hsp70 enhanced NF-kappaB activation, which was clearly inhibited by anti-TLR4, with the positive cell ratios being 67.44%, 39.17%, 31.56% and 28.05 %, respectively. TLR4 was rapidly down-regulated in the presence of hsp70. MFI of TLR4 on monocytes in different time points were 87.77 +/- 5.38, 78.16 +/- 6.01 and 45.17 +/- 4.97 (P<0.05), 26.98 +/- 5.83 (P<0.01), respectively. Moreover, hsp70-induced TNF-alpha production by human monocytes was inhibited by anti-TLR4. It is suggested that TLR4 is involved in the hsp70-mediated activation of innate immunity.
