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a Department of Anesthesiology, Heinrich Heine University, Düsseldorf, 40225, Germany b Centro de Estudios Farmacologicos y Botanicos, Consejo Nacional de Investigaciones Cientificas y Tecnicas, 1414 Buenos Aires, Argentina c Department of Urology, Carl Gustav Carus University Hospital, University of Dresden, Dresden, Germany d Department of Anaesthesiology, Heinrich Heine University, 40225 Düsseldorf, Germany
Key Words: toll-like receptors • knockout • bidirectional regulation • LPA
Address for correspondence: Prof. Dr. Stefan R. Bornstein, Department of Medicine III, Carl Gustav Carus Medical School, University of Technology, Dresden, Fetscherstrasse 74, 01307 Dresden, Germany. Voice: +49-351-458-5955; fax: +49-351-458-6398. e-mail: Stefan.Bornstein{at}uniklinikum-dresden.de
Sepsis and septic shock remain 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. Toll-like receptors (TLRs) are critical in the early immune response upon bacterial infection, and recent data from our lab demonstrate a novel link between the innate immune system and the adrenal stress response mediated by TLRs. Glucocorticoids and TLRs regulate each other in a bidirectional way. Bacterial toxins acting through TLRs directly activate adrenocortical steroid release. TLR-2 and TLR-4 are expressed in human and mice adrenals and TLR-2 deficiency is associated with an impaired glucocorticoid response. Furthermore, TLR-2 deficiency in mice is associated with marked cellular alterations in adrenocortical tissue. TLR-2-deficient mice have an impaired adrenal corticosterone release following inflammatory stress induced by bacterial cell wall compounds. This defect appears to be associated with a decrease in systemic and intraadrenal cytokine expression. In conclusion, TLRs play a crucial role in the immune–adrenal crosstalk. This close functional relationship needs to be considered in the treatment of inflammatory diseases requiring an intact adrenal stress response.
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