Impaired adrenal stress response in Toll-like receptor 2-deficient mice
| Autor: | Stefan R. Bornstein, Claudia Papewalis, Kai Zacharowski, Klaus Schulze-Osthoff, Nguyen Tran, Paula A. Zacharowski, Jörg Tarnow, Werner A. Scherbaum, Samuel M. McCann, Andreas Barthel, Valeria Rettori, Ralf R. Schumann |
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| Rok vydání: | 2004 |
| Předmět: |
Lipopolysaccharides
medicine.medical_specialty Receptors Cell Surface Adrenocorticotropic hormone Biology Models Biological Mice chemistry.chemical_compound Immune system Adrenocorticotropic Hormone Corticosterone Sepsis Internal medicine medicine Animals Humans Mice Knockout Toll-like receptor Multidisciplinary Innate immune system Adrenal cortex NF-kappa B Biological Sciences Endotoxemia Immunity Innate Toll-Like Receptor 2 Mice Inbred C57BL Teichoic Acids Endocrinology medicine.anatomical_structure chemistry Immunology Adrenal Cortex Cytokines Tumor necrosis factor alpha Glucocorticoid medicine.drug |
| Zdroj: | Proceedings of the National Academy of Sciences. 101:16695-16700 |
| ISSN: | 1091-6490 0027-8424 |
| Popis: | Septicemia is one of the major health concerns worldwide, and rapid activation of adrenal steroid release is a key event in the organism's first line of defense during this form of severe illness. The family of Toll-like receptors (TLRs) is critical in the early immune response upon bacterial infection, and TLR polymorphisms are frequent in humans. Here, we demonstrate that TLR-2 deficiency in mice is associated with reduced plasma corticosterone levels and marked cellular alterations in adrenocortical tissue. TLR-2-deficient mice have an impaired adrenal corticosterone release after inflammatory stress induced by bacterial cell wall compounds. This defect appears to be mediated by a decrease in systemic and intraadrenal cytokine expression, including IL-1, tumor necrosis factor α, and IL-6. Our data demonstrate a link between the innate immune system and the endocrine stress response. The critical role of TLR-2 in adrenal glucocorticoid regulation needs to be considered in patients with inflammatory disease. |
| Databáze: | OpenAIRE |
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