کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10455075 | 921068 | 2010 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Reduced cortisol levels in cerebrospinal fluid and differential distribution of 11β-hydroxysteroid dehydrogenases in multiple sclerosis: Implications for lesion pathogenesis
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کلمات کلیدی
dehydroepiandrosteroneSecondary Progressive MSDHEARelapsing-remitting MSSPMSRRMsEAEexperimental autoimmune encephalomyelitis - آنسفالومیلیت خودایمنی تجربیMRI - امآرآی یا تصویرسازی تشدید مغناطیسیMagnetic resonance imaging - تصویربرداری رزونانس مغناطیسیCNS - دستگاه عصبی مرکزیcentral nervous system - سیستم عصبی مرکزیMacrophages - ماکروفاژها،درشت خوارهاCSF - مایع مغزی نخاعیCerebrospinal fluid - مایع مغزی نخاعیMultiple sclerosis - مولتیپل اسکلروزیس(ام اس)HPA - میلی بار یا هکتوپاسکالhypothalamo–pituitary–adrenal - هیپوتالامو-هیپوفیز-آدرنالcortisol - کورتیزولGlucocorticoids - گلوکوکورتیکوئیدها
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Relapses during multiple sclerosis (MS) are treated by administration of exogenous corticosteroids. However, little is known about the bioavailability of endogenous steroids in the central nervous system (CNS) of MS patients. We thus determined cortisol and dehydroepiandrosterone (DHEA) levels in serum and cerebrospinal fluid (CSF) samples from 34 MS patients, 28 patients with non-inflammatory neurological diseases (NIND) and 16 patients with other inflammatory neurological diseases (OIND). This revealed that MS patients - in sharp contrast to patients with OIND - show normal cortisol concentrations in serum and lowered cortisol levels in the CSF during acute relapses. This local cortisol deficit may relate to poor local activation of cortisone via 11β-hydroxysteroid dehydrogenase type 1 (11bHSD1) or to inactivation via 11bHSD2. Accordingly, 11bHSD2 was found to be expressed within active plaques, whereas 11bHSD1 was predominantly detected in surrounding “foamy” macrophages. Our study thus provides new insights into the impaired endogenous CNS cortisol regulation in MS patients and its possible relation to MS lesion pathogenesis. Moreover, an observed upregulation of 11bHSD1 in myelin-loaded macrophages in vitro suggests an intriguing hypothesis for the self-limiting nature of MS lesion development. Finally, our findings provide an attractive explanation for the effectivity of high- vs. low-dose exogenous corticosteroids in the therapy of acute relapses.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain, Behavior, and Immunity - Volume 24, Issue 6, August 2010, Pages 975-984
Journal: Brain, Behavior, and Immunity - Volume 24, Issue 6, August 2010, Pages 975-984
نویسندگان
Claudia Heidbrink, Sebastian F.M. Häusler, Mathias Buttmann, Monika Ossadnik, Herwig M. Strik, Andreas Keller, Dorothea Buck, Evert Verbraak, Marjan van Meurs, Mathias Krockenberger, Matthias Mehling, Michel Mittelbronn, Jon D. Laman, Heinz Wiendl,