Interleukin 27 is increased in carotid atherosclerosis and promotes NLRP3 inflammasome activation
نویسندگان
چکیده
منابع مشابه
Interleukin 27 is increased in carotid atherosclerosis and promotes NLRP3 inflammasome activation
AIM Interleukin-27 (IL-27) is involved in different inflammatory diseases; however, its role in atherosclerosis is unclear. In this study we investigated the expression of IL-27 and its receptor in patients with carotid atherosclerosis and if IL-27 could modulate the inflammatory effects of the NLRP3 inflammasome in vitro. METHODS Plasma IL-27 was measured by enzyme immunoassay in patients wi...
متن کاملNLRP3 Inflammasome Expression and Activation in Human Atherosclerosis
BACKGROUND The NLR family, pyrin domain containing 3 (NLRP3) inflammasome is an interleukin (IL)-1β and IL-18 cytokine processing complex that is activated in inflammatory conditions. The role of the NLRP3 inflammasome in the pathogenesis of atherosclerosis and myocardial infarction is not fully understood. METHODS AND RESULTS Atherosclerotic plaques were analyzed for transcripts of the NLRP3...
متن کاملRIPK3 promotes cell death NLRP3 inflammasome and interleukin-1 activation in the absence of MLKL
RIPK3 and its substrate MLKL are essential for necroptosis, a lytic cell death proposed to cause inflammation via the release of intracellular molecules. Whether and how RIPK3 might drive inflammation in a manner independent of MLKL and cell lysis remains unclear. Here we show that following LPS treatment, or LPS-induced necroptosis, the TLR adaptor protein TRIF and IAPs (XIAP/cIAP1/cIAP2) regu...
متن کاملPKM2-dependent glycolysis promotes NLRP3 and AIM2 inflammasome activation
Sepsis, severe sepsis and septic shock are the main cause of mortality in non-cardiac intensive care units. Immunometabolism has been linked to sepsis; however, the precise mechanism by which metabolic reprogramming regulates the inflammatory response is unclear. Here we show that aerobic glycolysis contributes to sepsis by modulating inflammasome activation in macrophages. PKM2-mediated glycol...
متن کاملThe Adaptor MAVS Promotes NLRP3 Mitochondrial Localization and Inflammasome Activation
NLRP3 is a key component of the macromolecular signaling complex called the inflammasome that promotes caspase 1-dependent production of IL-1β. The adaptor ASC is necessary for NLRP3-dependent inflammasome function, but it is not known whether ASC is a sufficient partner and whether inflammasome formation occurs in the cytosol or in association with mitochondria is controversial. Here, we show ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: PLOS ONE
سال: 2017
ISSN: 1932-6203
DOI: 10.1371/journal.pone.0188387