توجه ! این یک نسخه آرشیو شده میباشد و در این حالت شما عکسی را مشاهده نمیکنید برای مشاهده کامل متن و عکسها بر روی لینک مقابل کلیک کنید : Regulation of IL-17 Family Members by Adrenal Hormones During Experimental Sepsis in Mice

محمد بهبهانی
04-10-2013, 02:56 PM
Severe sepsis is a life-threatening disease that causes major morbidity and mortality. Catecholamines
and glucocorticoids often have been used for the treatment of sepsis. Several recent studies have
suggested a potential role of IL-17 during the development and progression of sepsis in small animal
models. In this study, the cross-talk of catecholamines and glucocorticoids with members of the IL-17
family was investigated during sepsis in C57BL/6 mice. The concentrations in plasma of IL-17A, IL-17F,
and the IL-17AF heterodimer all were increased greatly in mice after endotoxemia or cecal ligation and
puncture as compared with sham mice. Surprisingly, when compared with IL-17A (487 pg/mL), the
concentrations of IL-17F (2361 pg/mL) and the heterodimer, IL-17AF (5116 pg/mL), were much higher
12 hours after endotoxemia. After surgical removal of the adrenal glands, mice had much higher
mortality after endotoxemia or cecal ligation and puncture. The absence of endogenous adrenal gland
hormones (cortical and medullary) was associated with 3- to 10-fold higher concentrations of IL-17A,
IL-17F, IL-17AF, and IL-23. The addition of adrenaline, noradrenaline, hydrocortisone, or dexamethasone
to lipopolysaccharide-activated peritoneal macrophages dose-dependently suppressed the
expression and release of IL-17s. The production of IL-17s required activation of c-Jun-N-terminal
kinase, which was antagonized by both catecholamines and glucocorticoids. These data provide novel
insights into the molecular mechanisms of immune modulation by catecholamines and glucocorticoids
during acute inflammation. (Am J Pathol 2013, 182: 1124e1130