کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2183988 | 1095611 | 2011 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Stimulation of Fas signaling down-regulates activity of neutrophils from major trauma patients with SIRS
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کلمات کلیدی
cellular FLICE-inhibitory proteinDHRGM-CSFFADDPMNphorbol 12-myristate 13-acetateFCSAISISSc-FLIPMOFMFIFITCFACSPBSMPO - DFOPMA - LDC هاMAPK - MAPKICU - بخش مراقبتهای ویژهintensive care unit - بخش مراقبتهای ویژهBase excess - بیش از حد پایهANOVA - تحلیل واریانس Analysis of varianceone-way analysis of variance - تحلیل واریانس یک راههEnzyme-linked immunosorbent assay - تست الیزاELISA - تست الیزاdihydrorhodamine - دی هیدرو رودامینfetal calf serum - سرم گوساله جنینMultiple organ failure - شکستگی اندام چندگانهFas Ligand - فاس لیگاندFasL - فاسدfluorescein isothiocyanate - فلوئورسین ایسوتیوسیاناتgranulocyte macrophage-colony stimulating factor - ماکروفاژ عصبی ماکروفاژ - colony stimulating factorPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریAbbreviated Injury Scale - مقیاس ضریب همبستگیmean fluorescence intensity - میانگین شدت فلورسانسmyeloperoxidase - میلوپراکسیداز Injury severity score - نمره شدت آسیبFAS-associated death domain protein - پروتئین دامنه مرگ مرتبط با FASmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenPropidium iodide - پروتئین یدید
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Posttrauma apoptosis resistance of neutrophils (PMN) is related to overshooting immune responses, systemic inflammatory response syndrome (SIRS) and multiple organ failure (MOF). Recently, we have shown that the apoptosis resistance in circulating PMN from severely injured patients which is known to be mediated by high serum levels of pro-inflammatory cytokines can be overcome by the activation of Fas death receptor. Here, we aimed to study whether stimulation of surface Fas leads to the inactivation of hyperactivated PMN from critically ill patients with SIRS. PMN from 23 multiple trauma patients (mean injury severity score (ISS) 34 ± 1.9) were isolated at day 1 after admission to the trauma center. PMN from 17 volunteer blood donors served as controls. Neutrophil activity has been determined after ex vivo short (1 h) and long-term (4 h) stimulation of freshly isolated PMN with immobilized agonistic anti-Fas antibodies. We found neutrophil chemotactic migration in response to IL-8, phagocytosis and oxidative burst to be significantly inhibited in control cells already after short-term (1 h) Fas stimulation. In contrast, inactivation of trauma PMN by agonistic anti-Fas antibodies was found to be efficient only after long-term (4 h) incubation of cells with agonistic antibodies. Thus, in trauma PMN down-regulation of neutrophil activity seems to be delayed when compared to cells isolated from healthy controls, suggesting impaired susceptibility for Fas stimulation in these cells. Interestingly, whereas Fas-mediated inhibition of phagocytosis and oxidative burst could be prevented by the broad range caspase inhibitor t-butoxycarbonyl-aspartyl(O-methyl)-fluoromethyl ketone (BocD-fmk), the chemotactic activity in response to IL-8 was unaffected. In conclusion, we demonstrate that stimulation of neutrophil Fas does not only initiate apoptosis but also induces inhibition of neutrophil functions, partially by non-apoptotic signaling.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Immunobiology - Volume 216, Issue 3, March 2011, Pages 334-342
Journal: Immunobiology - Volume 216, Issue 3, March 2011, Pages 334-342
نویسندگان
Adnana Paunel-Görgülü, Tim Lögters, Sascha Flohé, Jindrich Cinatl, Jens Altrichter, Joachim Windolf, Martin Scholz,