| First Author | Bornstein SR | Year | 2004 |
| Journal | Proc Natl Acad Sci U S A | Volume | 101 |
| Issue | 47 | Pages | 16695-700 |
| PubMed ID | 15546996 | Mgi Jnum | J:94463 |
| Mgi Id | MGI:3512839 | Doi | 10.1073/pnas.0407550101 |
| Citation | Bornstein SR, et al. (2004) Impaired adrenal stress response in Toll-like receptor 2-deficient mice. Proc Natl Acad Sci U S A 101(47):16695-700 |
| abstractText | 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 alpha, 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. |
