Data on microbial DNA-induced IL-1β production in monocytes of type 1 diabetes patients

被引:0
|
作者
Zentsova, Irena [1 ]
Parackova, Zuzana [1 ]
Kayserova, Jana [1 ]
Palova-Jelinkova, Lenka [5 ]
Vrabcova, Petra [1 ]
Volfova, Nikol [3 ,4 ]
Sumnik, Zdenek [2 ]
Pruhova, Stepanka [2 ]
Petruzelkova, Lenka [2 ]
Sediva, Anna [1 ]
机构
[1] Charles Univ Prague, Dept Immunol, Fac Med 2, Univ Hosp Motol, Prague, Czech Republic
[2] Charles Univ Prague, Dept Pediat, Fac Med 2, Univ Hosp Motol, Prague, Czech Republic
[3] Charles Univ Prague, Fac Med 1, Dept Pediat & Adolescent Med, Prague, Czech Republic
[4] Gen Univ Hosp, Prague, Czech Republic
[5] Sotio Ac, Prague, Czech Republic
来源
DATA IN BRIEF | 2019年 / 25卷
关键词
Type; 1; diabetes; Monocytes; DNA; Inflammasomes; Glybenclamide; NLRP3;
D O I
10.1016/j.dib.2019.104321
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Inflammasomes are large protein complexes involved in the maturation of IL-1 beta, a cytokine associated with the pathophysiology of type 1 diabetes (T1D). The data presented in this article focused on the role of inflammasomes in DNA recognition in T1D patients. This data extend knowledge on DNA sensing in T1D patients and relate to our research paper "Monocytes contribute to DNA sensing through the TBK1 signaling pathway in type 1 diabetes patients" Zentsova et al., 2009. To examine inflammasome involvement, we blocked the known mechanism of inflammasome activation - potassium efflux via various approaches: 1) high concentration of KCl; 2) Glybenclamide, which selectively blocks the ATP sensitive K+ channel; 3) KN-62, an inhibitor of P2X7 receptor, which activates K+ channel after ATP binding. Moreover, we used an inhibitor which blocks Nod-like receptor family containing pyrin domain 3 (NLRP3) inflammasome. In T1D patients, we show that secretion of cytokines IL-1 beta, TNF alpha, IL-6 and IFN alpha after microbial DNA stimulation is promoted by potassium efflux and is not dependent on P2X7 receptor signaling. Surprisingly, the microbial DNA induced IL-1 beta release was independent of NLRP3. (C) 2019 The Author(s). Published by Elsevier Inc.
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页数:5
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