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Interleukin-33

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https://www.readbyqxmd.com/read/29346765/characterization-of-endothelial-cells-associated-with-hematopoietic-niche-formation-in-humans-identifies-il-33-as-an-anabolic-factor
#1
Keane Jared Guillaume Kenswil, Adrian Christopher Jaramillo, Zhen Ping, Si Chen, Remco Michiel Hoogenboezem, Maria Athina Mylona, Maria Niken Adisty, Eric Moniqué Johannes Bindels, Pieter Koen Bos, Hans Stoop, King Hong Lam, Bram van Eerden, Tom Cupedo, Marc Hermanus Gerardus Petrus Raaijmakers
Bone marrow formation requires an orchestrated interplay between osteogenesis, angiogenesis, and hematopoiesis that is thought to be mediated by endothelial cells. The nature of the endothelial cells and the molecular mechanisms underlying these events remain unclear in humans. Here, we identify a subset of endoglin-expressing endothelial cells enriched in human bone marrow during fetal ontogeny and upon regeneration after chemotherapeutic injury. Comprehensive transcriptional characterization by massive parallel RNA sequencing of these cells reveals a phenotypic and molecular similarity to murine type H endothelium and activation of angiocrine factors implicated in hematopoiesis, osteogenesis, and angiogenesis...
January 16, 2018: Cell Reports
https://www.readbyqxmd.com/read/29346528/a-novel-stromal-lncrna-signature-reprograms-fibroblasts-to-promote-the-growth-of-oral-squamous-cell-carcinoma-via-lncrna-caf-interleukin-33
#2
Liang Ding, Jing Ren, Dongya Zhang, Yi Li, Xiaofeng Huang, Qingang Hu, Hui Wang, Yuxian Song, Yanhong Ni, Yayi Hou
Stromal carcinoma-related fibroblasts (CAFs) are the main type of non-immune cells in the tumor microenvironment (TME). CAFs interact with cancer cells to promote tumor proliferation. Long non-coding RNAs (lncRNAs) are known to regulate cell growth, apoptosis, and metastasis of cancer cells, but their role in stromal cells is unclear. Using RNA sequencing, we identified a stromal lncRNA signature during the transformation of CAFs from normal fibroblasts (NFs) in oral squamous cell carcinoma (OSCC). We uncovered an uncharacterized lncRNA, FLJ22447, which was remarkably up-regulated in CAFs, referred to LncRNA-CAF (Lnc-CAF) hereafter...
January 13, 2018: Carcinogenesis
https://www.readbyqxmd.com/read/29331644/ozone-exposure-induces-respiratory-barrier-biphasic-injury-and-inflammation-controlled-by-interleukin-33
#3
Chloé Michaudel, Claire Mackowiak, Isabelle Maillet, Louis Fauconnier, Cezmi Akdis, Milena Sokolowska, Anita Dreher, Hern-Tze Tina Tan, Valérie F Quesniaux, Bernhard Ryffel, Dieudonnée Togbe
BACKGROUND: IL-33 plays critical role in the regulation of tissue homeostasis, injury and repair. Whether IL-33 regulates neutrophil recruitment and function independently of airways hyperresponsiveness (AHR) in ozone induced lung injury and inflammation is unclear. OBJECTIVE: To examine the role of IL-33/ST2 axis in lung inflammation upon acute ozone exposure in mice. METHODS: ST2 and IL-33 deficient mice, IL-33-citrine reporter and C57BL/6 (WT) mice underwent a single ozone exposure (1 ppm for 1h) in all studies...
January 10, 2018: Journal of Allergy and Clinical Immunology
https://www.readbyqxmd.com/read/29329638/role-of-the-il-33-st2l-axis-in-colorectal-cancer-progression
#4
Miho Akimoto, Keizo Takenaga
Interleukin-33 (IL-33) has been identified as a natural ligand of ST2L. IL-33 primarily acts as a key regulator of Th2 responses through binding to ST2L, which is antagonized by soluble ST2 (sST2). The IL-33/ST2L axis is involved in various inflammatory pathologies, including ulcerative colitis (UC). Several recent investigations have also suggested that the IL-33/ST2L axis plays a role in colorectal cancer (CRC) progression. In CRC, tumor- and stroma-derived IL-33 may activate ST2L on various cell types in an autocrine and paracrine manner...
January 9, 2018: Cellular Immunology
https://www.readbyqxmd.com/read/29329586/il-33-st2-signaling-contributes-to-radicular-pain-by-modulating-mapk-and-nf-%C3%AE%C2%BAb-activation-and-inflammatory-mediator-expression-in-the-spinal-cord-in-rat-models-of-noncompressive-lumber-disk-herniation
#5
Si-Jian Huang, Jian-Qin Yan, Hui Luo, Lu-Yao Zhou, Jian-Gang Luo
BACKGROUND: Immune and inflammatory responses occurring in the spinal cord play a pivotal role in the progression of radicular pain caused by intervertebral disk herniation. Interleukin-33 (IL-33) orchestrates inflammatory responses in a wide range of inflammatory and autoimmune disorders of the nervous system. Thus, the purpose of this study is to investigate the expression of IL-33 and its receptor ST2 in the dorsal spinal cord and to elucidate whether the inhibition of spinal IL-33 expression significantly attenuates pain-related behaviors in rat models of noncompressive lumbar disc herniation...
January 12, 2018: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29325227/soluble-st2-in-end-stage-heart-failure-before-and-after-support-with-a-left-ventricular-assist-device
#6
C C S Tseng, M M H Huibers, L H Gaykema, E Siera-de Koning, F Z Ramjankhan, A S Maisel, N de Jonge
BACKGROUND: The interleukin-33 (IL-33)/supressor of tumorigenicity 2 (ST2) pathway is suggested to play an important role in fibrosis, remodeling and the progression of heart failure (HF). Increased soluble (sST2) levels are associated with adverse outcome in the average HF population. Less is known about sST2 levels in end-stage HF. Therefore, we studied sST2 levels in end-stage HF and the effect of unloading by left ventricular assist device (LVAD) support on sST2 levels. METHOD AND RESULTS: Serial plasma measurements of sST2 were performed pre-implantation and 1, 3 and 6 months after (LVAD) implantation in 38 patients...
January 11, 2018: European Journal of Clinical Investigation
https://www.readbyqxmd.com/read/29306406/what-is-the-role-of-interleukin-33-and-st2-receptor-in-myasthenia-gravis
#7
Izabela Monika Rozmilowska, Monika Helena Adamczyk-Sowa
No abstract text is available yet for this article.
February 15, 2018: Journal of Neuroimmunology
https://www.readbyqxmd.com/read/29285671/the-interleukin-33-st2-pathway-is-expressed-in-the-failing-human-heart-and-associated-with-pro-fibrotic-remodeling-of-the-myocardium
#8
Cheyenne C S Tseng, Manon M H Huibers, Joyce van Kuik, Roel A de Weger, Aryan Vink, Nicolaas de Jonge
The interleukin-33 (IL-33)/suppression of tumorigenicity 2 (ST2) pathway is a potential pathophysiological mediator of cardiac fibrosis. Soluble ST2 (sST2) is one of the main isoforms of ST2 with strong prognostic value in cardiac disease. The exact role of sST2 in cardiac fibrosis is unknown. The aim of this study was (1) to investigate myocardial expression of the IL-33/ST2 pathway in relation to myocardial fibrosis in end-stage heart failure patients and (2) to study whether plasma sST2 is associated with histologically determined cardiac fibrosis...
December 28, 2017: Journal of Cardiovascular Translational Research
https://www.readbyqxmd.com/read/29283120/correlation-of-interleukin-33-with-th-cytokines-and-clinical-severity-of-dry-eye-disease
#9
Guoping Luo, Yan Xin, Dajun Qin, Aihua Yan, Zhiyan Zhou, Zhaoxia Liu
PURPOSE: The purpose of this study is to determine the tear and serum protein levels of interleukin-33 (IL-33) and its correlation with Th cytokines and disease severity in dry eye (DE) syndrome. METHODS: Tear and serum samples were collected from 30 healthy volunteers, 30 DE patients with non-Sjogren's syndrome DE (NSSDE) and 30 DE patients with primary SSDE. The eight most frequent symptoms of DE were scored. All patients underwent corneal and conjunctival staining, tear film breakup time (TBUT), and Schirmer I test...
January 2018: Indian Journal of Ophthalmology
https://www.readbyqxmd.com/read/29247993/interleukin-33-il-33-a-nuclear-cytokine-from-the-il-1-family
#10
REVIEW
Corinne Cayrol, Jean-Philippe Girard
Interleukin-33 (IL-33) is a tissue-derived nuclear cytokine from the IL-1 family abundantly expressed in endothelial cells, epithelial cells and fibroblast-like cells, both during homeostasis and inflammation. It functions as an alarm signal (alarmin) released upon cell injury or tissue damage to alert immune cells expressing the ST2 receptor (IL-1RL1). The major targets of IL-33 in vivo are tissue-resident immune cells such as mast cells, group 2 innate lymphoid cells (ILC2s) and regulatory T cells (Tregs)...
January 2018: Immunological Reviews
https://www.readbyqxmd.com/read/29208683/il-33-and-st2-mediate-fak-dependent-antitumor-immune-evasion-through-transcriptional-networks
#11
Bryan Serrels, Niamh McGivern, Marta Canel, Adam Byron, Sarah C Johnson, Henry J McSorley, Niall Quinn, David Taggart, Alex Von Kreigsheim, Stephen M Anderton, Alan Serrels, Margaret C Frame
Focal adhesion kinase (FAK) mediates tumor cell-intrinsic behaviors that promote tumor growth and metastasis. We previously showed that FAK also induces the expression of inflammatory genes that inhibit antitumor immunity in the microenvironment. We identified a crucial, previously unknown role for the dual-function cytokine interleukin-33 (IL-33) in FAK-dependent immune evasion. In murine squamous cell carcinoma (SCC) cells, specifically nuclear FAK enhanced the expression of the genes encoding IL-33, the chemokine CCL5, and the soluble, secreted form of the IL-33 receptor, called soluble ST2 (sST2)...
December 5, 2017: Science Signaling
https://www.readbyqxmd.com/read/29206477/acute-eosinophilic-pneumonia-causes-diagnosis-and-management
#12
Federica De Giacomi, Robert Vassallo, Eunhee S Yi, Jay H Ryu
Acute eosinophilic pneumonia is an uncommon acute respiratory illness of varying severity that includes presentation as acute respiratory distress syndrome with fatal outcome. Acute eosinophilic pneumonia may be idiopathic but identifiable causes include smoking and other inhalational exposures, medications and infections. The pathogenesis of acute eosinophilic pneumonia is poorly understood but likely varies depending on the underlying cause. Airway epithelial injury, endothelial injury and release of interleukin-33 are early events that subsequently promote eosinophil recruitment to the lung; eosinophilic infiltration and degranulation appear to mediate subsequent lung inflammation and associated clinical manifestations...
December 5, 2017: American Journal of Respiratory and Critical Care Medicine
https://www.readbyqxmd.com/read/29204432/caspase-1-deficiency-reduces-eosinophilia-and-interleukin-33-in-an-asthma-exacerbation-model
#13
Mandy Menzel, Hamid Akbarshahi, Irma Mahmutovic Persson, Manoj Puthia, Leif Bjermer, Lena Uller
Rhinovirus infections are common triggers of asthma exacerbations. Viruses can activate the inflammasome, resulting in processing and activation of caspase-1. This recruitment triggers production of interleukin (IL)-1β and IL-18, which have been implicated in asthma. Elucidating the involvement of the inflammasome and its compartments, such as caspase-1, in asthma exacerbations is warranted. Gene expression of caspase-1 was measured in rhinovirus-infected primary bronchial epithelial cells of asthmatic and healthy donors 24 h post-infection...
October 2017: ERJ Open Research
https://www.readbyqxmd.com/read/29197857/corrigendum-to-interleukin-33-plasma-levels-in-patients-with-relapsing-remitting-multiple-sclerosis
#14
Fereshteh Alsahebfosoul, Ilnaz Rahimmanesh, Mansour Shajarian, Masoud Etemadifar, Nahid Sedaghat, Zahra Hejazi, Shamsi Naderi
No abstract text is available yet for this article.
December 4, 2017: Biomolecular Concepts
https://www.readbyqxmd.com/read/29190116/alarmins-in-frozen-shoulder-a-molecular-association-between-inflammation-and-pain
#15
Jonathon Z B Cher, Moeed Akbar, Susan Kitson, Lindsay A N Crowe, Emma Garcia-Melchor, Stephen C Hannah, Michael McLean, Umberto G Fazzi, Shauna C Kerr, George A C Murrell, Neal L Millar
BACKGROUND: The pathophysiological mechanisms behind proliferation of fibroblasts and deposition of dense collagen matrix in idiopathic frozen shoulder remain unclear. Alarmins (also known as danger signals) are endogenous molecules that are released into the extracellular milieu after infection or tissue injury and that signal cell and tissue damage. PURPOSE: To investigate whether the presence of alarmins is higher in patients with idiopathic frozen shoulder than in control subjects...
November 1, 2017: American Journal of Sports Medicine
https://www.readbyqxmd.com/read/29186722/il-33-expression-in-chronic-rhinosinusitis-with-nasal-polyps-and-its-relationship-with-clinical-severity
#16
Wei Song, Chunlei Wang, Jing Zhou, Shenghua Pan, Sen Lin
BACKGROUND: Chronic rhinosinusitis (CRS) is a heterogeneous disease characterized by epithelial inflammation and tissue eosinophilic infiltration. Interleukin-33 (IL-33) is a key inflammatory cytokine that mediates eosinophilic infiltration. OBJECTIVE: The aim of our study was to investigate the expression and role of IL-33 in eosinophilic CRS with nasal polyps (ECRSwNP) and in noneosinophilic CRS with nasal polyps (nECRSwNP), and to analyze their correlation with clinical severity...
November 30, 2017: ORL; Journal for Oto-rhino-laryngology and its related Specialties
https://www.readbyqxmd.com/read/29180837/il-33-st2-axis-in-liver-disease-progression-and-challenge
#17
REVIEW
Zijian Sun, Binxia Chang, Miaomiao Gao, Jiyuan Zhang, Zhengsheng Zou
The new member of the IL-1 family, interleukin-33 (IL-33), participates in the progression of a variety of diseases through binding with its receptor ST2. Recently, much clinical evidence and experimental data have indicated that IL-33 is associated with various liver diseases. This review primarily addresses the relationship between IL-33 and several hepatic diseases. IL-33 can alleviate high-fat diet- (HFD-) induced hepatic steatosis and insulin resistance, and IL-33 acts as an alarmin, which quickly triggers the immune system to respond to virus invasion and toxic damage to the liver...
2017: Mediators of Inflammation
https://www.readbyqxmd.com/read/29175156/il-33-st2-pathway-as-a-rational-therapeutic-target-for-cns-diseases
#18
REVIEW
Li-Xia Du, Yan-Qing Wang, Guo-Qiang Hua, Wen-Li Mi
Interleukin-33 (IL-33) is a member of the interleukin-1 cytokine family that is produced by many different types of tissues including the central nervous system (CNS). IL-33 mediates its effects via its heterodimeric receptor complex, comprised of ST2 and the IL-1 receptor accessory protein (IL-1RAcp). As a pleiotropic nuclear cytokine, IL-33 is a crucial actor in the development of cardiovascular diseases, allergic diseases, infectious diseases, and autoimmune diseases. Recently, accumulated evidence show that the IL-33/ST2 axis plays a crucial and diverse role in the pathogenesis of CNS diseases, including neurodegenerative diseases, cerebrovascular diseases, infectious diseases, traumatic CNS injury, chronic pain, etc...
November 23, 2017: Neuroscience
https://www.readbyqxmd.com/read/29166590/interleukin-33-activated-islet-resident-innate-lymphoid-cells-promote-insulin-secretion-through-myeloid-cell-retinoic-acid-production
#19
Elise Dalmas, Frank M Lehmann, Erez Dror, Stephan Wueest, Constanze Thienel, Marcela Borsigova, Marc Stawiski, Emmanuel Traunecker, Fabrizio C Lucchini, Dianne H Dapito, Sandra M Kallert, Bruno Guigas, Francois Pattou, Julie Kerr-Conte, Pierre Maechler, Jean-Philippe Girard, Daniel Konrad, Christian Wolfrum, Marianne Böni-Schnetzler, Daniela Finke, Marc Y Donath
Pancreatic-islet inflammation contributes to the failure of β cell insulin secretion during obesity and type 2 diabetes. However, little is known about the nature and function of resident immune cells in this context or in homeostasis. Here we show that interleukin (IL)-33 was produced by islet mesenchymal cells and enhanced by a diabetes milieu (glucose, IL-1β, and palmitate). IL-33 promoted β cell function through islet-resident group 2 innate lymphoid cells (ILC2s) that elicited retinoic acid (RA)-producing capacities in macrophages and dendritic cells via the secretion of IL-13 and colony-stimulating factor 2...
November 21, 2017: Immunity
https://www.readbyqxmd.com/read/29166583/the-skinny-pancreatic-ilc2s-promote-insulin-secretion
#20
Kelly M Cautivo, Ari B Molofsky
Regulation of pancreatic insulin production is pivotal in the pathophysiology and treatment of diabetes. In this issue of Immunity, Dalmas et al. (2017) describe a type 2 immune circuit where pancreatic interleukin-33 (IL-33) promotes insulin secretion via the activity of islet-associated group 2 innate lymphoid cells (ILC2s).
November 21, 2017: Immunity
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