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Statements

Subject Item
n2:RIV%2F00216208%3A11120%2F13%3A43907500%21RIV14-MSM-11120___
rdf:type
n11:Vysledek skos:Concept
dcterms:description
Celiac disease (CD) is a gluten-responsive, chronic inflammatory enteropathy. IL-1 cytokine family members IL-1 beta and IL-18 have been associated with the inflammatory conditions in CD patients. However, the mechanisms of IL-1 molecule activation in CD have not yet been elucidated. We show in this study that peripheral blood mononuclear cells (PBMC) and monocytes from celiac patients responded to pepsin digest of wheat gliadin fraction (PDWGF) by a robust secretion of IL-1 beta and IL-1 alpha and a slightly elevated production of IL-18. The analysis of the upstream mechanisms underlying PDWGF-induced IL-1 beta production in celiac PBMC show that PDWGF-induced de novo pro-IL-1 beta synthesis, followed by a caspase-1 dependent processing and the secretion of mature IL-1 beta. This was promoted by K+ efflux and oxidative stress, and was independent of P2X7 receptor signaling. The PDWGF-induced IL-1 beta release was dependent on Nod-like receptor family containing pyrin domain 3 (NLRP3) and apoptosis-associated speck like protein (ASC) as shown by stimulation of bone marrow derived dendritic cells (BMDC) from NLRP3(-/-) and ASC(-/-) knockout mice. Moreover, treatment of human PBMC as well as MyD88(-/-) and Toll-interleukin-1 receptor domain-containing adaptor-inducing interferon-beta (TRIF)(-/-) BMDC illustrated that prior to the activation of caspase-1, the PDWGF-triggered signal constitutes the activation of the MyD88/TRIF/MAPK/NF-kappa B pathway. Moreover, our results indicate that the combined action of TLR2 and TLR4 may be required for optimal induction of IL-1 beta in response to PDWGF. Thus, innate immune pathways, such as TLR2/4/MyD88/TRIF/MAPK/NF-kB and an NLRP3 inflammasome activation are involved in wheat proteins signaling and may play an important role in the pathogenesis of CD. Celiac disease (CD) is a gluten-responsive, chronic inflammatory enteropathy. IL-1 cytokine family members IL-1 beta and IL-18 have been associated with the inflammatory conditions in CD patients. However, the mechanisms of IL-1 molecule activation in CD have not yet been elucidated. We show in this study that peripheral blood mononuclear cells (PBMC) and monocytes from celiac patients responded to pepsin digest of wheat gliadin fraction (PDWGF) by a robust secretion of IL-1 beta and IL-1 alpha and a slightly elevated production of IL-18. The analysis of the upstream mechanisms underlying PDWGF-induced IL-1 beta production in celiac PBMC show that PDWGF-induced de novo pro-IL-1 beta synthesis, followed by a caspase-1 dependent processing and the secretion of mature IL-1 beta. This was promoted by K+ efflux and oxidative stress, and was independent of P2X7 receptor signaling. The PDWGF-induced IL-1 beta release was dependent on Nod-like receptor family containing pyrin domain 3 (NLRP3) and apoptosis-associated speck like protein (ASC) as shown by stimulation of bone marrow derived dendritic cells (BMDC) from NLRP3(-/-) and ASC(-/-) knockout mice. Moreover, treatment of human PBMC as well as MyD88(-/-) and Toll-interleukin-1 receptor domain-containing adaptor-inducing interferon-beta (TRIF)(-/-) BMDC illustrated that prior to the activation of caspase-1, the PDWGF-triggered signal constitutes the activation of the MyD88/TRIF/MAPK/NF-kappa B pathway. Moreover, our results indicate that the combined action of TLR2 and TLR4 may be required for optimal induction of IL-1 beta in response to PDWGF. Thus, innate immune pathways, such as TLR2/4/MyD88/TRIF/MAPK/NF-kB and an NLRP3 inflammasome activation are involved in wheat proteins signaling and may play an important role in the pathogenesis of CD.
dcterms:title
Pepsin Digest of Wheat Gliadin Fraction Increases Production of IL-1 beta via TLR4/MyD88/TRIF/MAPK/NF-kappa B Signaling Pathway and an NLRP3 Inflammasome Activation Pepsin Digest of Wheat Gliadin Fraction Increases Production of IL-1 beta via TLR4/MyD88/TRIF/MAPK/NF-kappa B Signaling Pathway and an NLRP3 Inflammasome Activation
skos:prefLabel
Pepsin Digest of Wheat Gliadin Fraction Increases Production of IL-1 beta via TLR4/MyD88/TRIF/MAPK/NF-kappa B Signaling Pathway and an NLRP3 Inflammasome Activation Pepsin Digest of Wheat Gliadin Fraction Increases Production of IL-1 beta via TLR4/MyD88/TRIF/MAPK/NF-kappa B Signaling Pathway and an NLRP3 Inflammasome Activation
skos:notation
RIV/00216208:11120/13:43907500!RIV14-MSM-11120___
n11:predkladatel
n16:orjk%3A11120
n3:aktivita
n7:P n7:I
n3:aktivity
I, P(GA310/07/0414), P(GA310/09/1640)
n3:cisloPeriodika
4
n3:dodaniDat
n13:2014
n3:domaciTvurceVysledku
n6:2905140 n6:9006214 n6:7735200
n3:druhVysledku
n12:J
n3:duvernostUdaju
n19:S
n3:entitaPredkladatele
n15:predkladatel
n3:idSjednocenehoVysledku
95701
n3:idVysledku
RIV/00216208:11120/13:43907500
n3:jazykVysledku
n14:eng
n3:klicovaSlova
gluten; secretion; nitric-oxide; immune-response; dendritic cells; blood monocytes; caspase-1 activation; differential requirement; celiac-disease; toll-like receptor
n3:klicoveSlovo
n4:differential%20requirement n4:nitric-oxide n4:gluten n4:blood%20monocytes n4:celiac-disease n4:secretion n4:immune-response n4:caspase-1%20activation n4:dendritic%20cells n4:toll-like%20receptor
n3:kodStatuVydavatele
US - Spojené státy americké
n3:kontrolniKodProRIV
[99BD2CF95E9F]
n3:nazevZdroje
PLoS One
n3:obor
n18:EB
n3:pocetDomacichTvurcuVysledku
3
n3:pocetTvurcuVysledku
12
n3:projekt
n10:GA310%2F09%2F1640 n10:GA310%2F07%2F0414
n3:rokUplatneniVysledku
n13:2013
n3:svazekPeriodika
8
n3:tvurceVysledku
Fundová, Petra Kotrbová - Kozak, Anna Katarzyna Černá, Marie
n3:wos
000321662800044
s:issn
1932-6203
s:numberOfPages
11
n5:organizacniJednotka
11120