Differential Regulation of Proinflammatory Mediators Following LPS- and ATP-Induced Activation of Monocytes from Patients with Antiphospholipid Syndrome

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61989592%3A15110%2F15%3A33154232" target="_blank" >RIV/61989592:15110/15:33154232 - isvavai.cz</a>

Výsledek na webu

<a href="http://www.hindawi.com/journals/bmri/2015/292851/" target="_blank" >http://www.hindawi.com/journals/bmri/2015/292851/</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1155/2015/292851" target="_blank" >10.1155/2015/292851</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Differential Regulation of Proinflammatory Mediators Following LPS- and ATP-Induced Activation of Monocytes from Patients with Antiphospholipid Syndrome

Popis výsledku v původním jazyce

Antiphospholipid syndrome (APS) is an acquired autoimmune disorder characterized by recurrent thrombosis and pregnancy morbidity in association with the presence of antiphospholipid antibodies. Growing evidence supports the involvement of monocytes in APS pathogenesis. Inflammatory activation of monocytes promotes thrombus formation and other APS complications. However, mechanisms underlying their activation are poorly investigated. We aimed to determine transcriptional activity of monocytes after exposing them to low concentrations of lipopolysaccharide (LPS) and LPS + adenosine triphosphate (ATP) using comparative qRT-PCR. The results showed that LPS significantly increased transcriptional levels of TLR2, IL-23, CCL2, CXCL10, IL-1?, and IL-6 in APS cells, while, in cells from healthy donors, LPS resulted in IL-6 and STAT3 elevated mRNAs. Double stimulation of the cells resulted in decreased mRNA levels of NLRP3 in monocytes isolated from healthy donors and CCL2, IL-1? in APS cells. B

Název v anglickém jazyce

Differential Regulation of Proinflammatory Mediators Following LPS- and ATP-Induced Activation of Monocytes from Patients with Antiphospholipid Syndrome

Popis výsledku anglicky

Antiphospholipid syndrome (APS) is an acquired autoimmune disorder characterized by recurrent thrombosis and pregnancy morbidity in association with the presence of antiphospholipid antibodies. Growing evidence supports the involvement of monocytes in APS pathogenesis. Inflammatory activation of monocytes promotes thrombus formation and other APS complications. However, mechanisms underlying their activation are poorly investigated. We aimed to determine transcriptional activity of monocytes after exposing them to low concentrations of lipopolysaccharide (LPS) and LPS + adenosine triphosphate (ATP) using comparative qRT-PCR. The results showed that LPS significantly increased transcriptional levels of TLR2, IL-23, CCL2, CXCL10, IL-1?, and IL-6 in APS cells, while, in cells from healthy donors, LPS resulted in IL-6 and STAT3 elevated mRNAs. Double stimulation of the cells resulted in decreased mRNA levels of NLRP3 in monocytes isolated from healthy donors and CCL2, IL-1? in APS cells. B

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

EC - Imunologie

OECD FORD obor

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Projekt

<a href="/cs/project/EE2.3.30.0004" target="_blank" >EE2.3.30.0004: Podpora vytváření excelentních výzkumných týmů a intersektorální mobility na Univerzitě Palackého v Olomouci</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>S - Specificky vyzkum na vysokych skolach

Rok uplatnění

2015

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

BioMed Research International

ISSN

2314-6133

e-ISSN

—

Svazek periodika

2015

Číslo periodika v rámci svazku

292851

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

9

Strana od-do

1-9

Kód UT WoS článku

000350581400001

EID výsledku v databázi Scopus

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