کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5896639 | 1568729 | 2016 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Sickle red cells as danger signals on proinflammatory gene expression, leukotriene B4 and interleukin-1 beta production in peripheral blood mononuclear cell
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کلمات کلیدی
HBFNod-like receptor family, pyrin domain containing 3High-mobility group protein B1apoptosis-associated speck-like protein containing CARDNLRP3LTB4NLRPBMCHMGB1TLRIL-1βDAMPsSCDASCSCARBCPAMPNLRP3 inflammasome - التهاب NLRP3pathogen-associated molecular pattern - الگوی مولکولی وابسته به پاتوژنSickle cell disease - بیماری سلول داسی شکلperipheral blood mononuclear cells - سلول های تک هسته ای خون محیطیLeukotriene B4 - لوکوترین B4Leukotriene - لکوترینFetal hemoglobin - هموگلوبین جنینیHydroxyurea - هیدروکسی اورهSickle cell anemia - کم خونی سلولی شکمred blood cell - گلبول قرمز، اریتروسیتNOD-like receptors - گیرنده های NOD مانندToll-like receptors - گیرنده های پولی مانند
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
علوم غدد
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Sickle red cells as danger signals on proinflammatory gene expression, leukotriene B4 and interleukin-1 beta production in peripheral blood mononuclear cell Sickle red cells as danger signals on proinflammatory gene expression, leukotriene B4 and interleukin-1 beta production in peripheral blood mononuclear cell](/preview/png/5896639.png)
چکیده انگلیسی
This study tested the hypothesis that sickle red blood cell (SS-RBC) induce Toll-like receptors (TLR) and Nod-like receptor family, pyrin domain containing 3 (NLRP3)- inflammasome expression in peripheral blood mononuclear cells (PBMC). TLR and NLRP3 inflammasome could contribute to the maintenance of the inflammatory status in sickle cell anemia (SCA) patients, since SS-RBC act as danger signals activating these pathways. In this study, first, we evaluated TLR (2, 4, 5 and 9), NLRP3, Caspase-1, interleukin (IL)-1β and IL-18 expression in PBMC freshly isolated from SCA patients (SS-PBMC) in comparison with PBMC from healthy individuals (AA-PBMC). In the second moment, we investigated whether SS-RBC could interfere with the expression of these molecules in PBMC from healthy donor, in the absence or presence of hydroxyurea (HU) in vitro. TLRs and NLRP3 inflammasome expression were investigated by qPCR. IL-1β, Leukotriene-B4 (LTB4) and nitrite production were measured in PBMC (from healthy donor) culture supernatants. TLR2, TLR4, TLR5, NLRP3 and IL-1β were highly expressed in SS-PBMC when compared to AA-PBMC. Additionally, SS-RBC induced TLR9, NLRP3, Caspase-1, IL-1β and IL-18 expression and induced IL-1β, LTB4 and nitrite production in PBMC cultures. HU did not prevent TLR and NLRP3 inflammasome expression, but increased TLR2 and IL-18 expression and reduced nitrite production. In conclusion, our data suggest that TLR and inflammasome complexes may be key inducers of inflammation in SCA patients, probably through SS-RBC; also, HU does not prevent NLRP3 inflammasome- and TLR-dependent inflammation, indicating the need to develop new therapeutic strategies to SCA patients that act with different mechanisms of those observed for HU.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cytokine - Volume 83, July 2016, Pages 75-84
Journal: Cytokine - Volume 83, July 2016, Pages 75-84
نویسندگان
Thassila N. Pitanga, Ricardo R. Oliveira, Dalila L. Zanette, Caroline C. Guarda, Rayra P. Santiago, Sanzio S. Santana, Valma M.L. Nascimento, Jonilson B. Lima, Graziele Q. Carvalho, Vitor V. Maffili, Magda O.S. Carvalho, Luiz C.J. Alcântara,