Differential expression and action of Toll-like receptors in human adrenocortical cells

被引:30
作者
Kanczkowski, Waldemar [1 ]
Zacharowski, Kai [2 ]
Wirth, Manfred P. [3 ]
Ehrhart-Bornstein, Monika [1 ]
Bornstein, Stefan R. [1 ]
机构
[1] Tech Univ Dresden, Carl Gustav Carus Univ Hosp, Dept Med, D-01307 Dresden, Germany
[2] Univ Hosp Bristol NHS Fdn Trust, Mol Cardioprotect & Inflammat Grp, Bristol BS2 8HW, Avon, England
[3] Tech Univ Dresden, Carl Gustav Carus Univ Hosp, Dept Urol, D-01307 Dresden, Germany
关键词
Immune-adrenal crosstalk; Inflammation; Cytokines; NF-kappa B activation; Stress response; Adrenal insufficiency; HUMAN ADRENAL-CELLS; STRESS-RESPONSE; MESSENGER-RNA; INFLAMMATION; SECRETION; INFECTION; CYTOKINES; IMMUNITY; SEPSIS; INNATE;
D O I
10.1016/j.mce.2008.10.028
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
During sepsis, an intact adrenal gland glucocorticoid stress response is critical for survival. Recently, we have shown that Toll-like receptors, particularly TLR2 and TLR4, are crucial in HPA axis regulation following inflammation, establishing a direct link between bacterial and viral ligands and the endocrine stress response. However, the exact role which TLRs play in adrenal homeostasis and malfunction is not yet sufficiently known. Using quantitative real-time PCR, confocal microscopy and the NF-kappa B reporter gene assay, we aimed to analyse both, expression and function of all relevant TLRs in the human adrenocortical cell line-NCl-H295R and adrenal cells in primary culture. Our results demonstrate a differential expression pattern of TLR1-9 in human adrenocortical cells as compared to immune cells and adrenocortical cancer cells. Consequently, activation of these cells by bacterial ligands leads to differential induction of cytokines including IL6, IL8 and TNF-alpha. Therefore, Toll-like receptors expression and function is a novel feature of the adrenal stress system contributing to adrenal tissue homeostasis, regeneration and tumorigenesis. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:57 / 65
页数:9
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