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Bornstein, S.R.* ; Zacharowski, P.A.* ; Schumann, R.R.* ; Barthel, A.* ; Tran, N.* ; Papewalis, C.* ; Rettori, V.* ; McCann, S.M.* ; Schulze-Osthoff, K.* ; Scherbaum, W.A.* ; Tarnow, J.* ; Zacharowski, K.*

Impaired adrenal stress response in Toll-like receptor 2-deficient mice.

Proc. Natl. Acad. Sci. U.S.A. 101, 16695-16700 (2004)

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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.

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