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IL-33 ST2

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https://www.readbyqxmd.com/read/29161088/mechanistic-basis-for-obesity-related-increases-in-ozone-induced-airway-hyperresponsiveness-in-mice
#1
Stephanie A Shore
Obesity is a risk factor for asthma, especially nonallergic asthma. Ozone, a common air pollutant, is a nonallergic asthma trigger. Importantly, ozone-induced decrements in lung function are greater in obese and overweight human subjects than in lean individuals. Obese mice also exhibit exaggerated pulmonary responses to ozone. Ozone causes greater increases in pulmonary resistance, in bronchoalveolar lavage neutrophils, and in airway hyperresponsiveness in obese than in lean mice. Our data indicate that IL-33 plays a role in mediating these events...
November 2017: Annals of the American Thoracic Society
https://www.readbyqxmd.com/read/29153199/soluble-st2-in-heart-failure
#2
REVIEW
Cian P McCarthy, James L Januzzi
Suppression of tumorigenicity 2 (ST2) is a member of the interleukin (IL)-1 receptor family, whose role was originally established in the context of inflammatory and autoimmune diseases. More recently, testing for ST2 has been used in the setting of cardiovascular disease. The soluble form of ST2 is a decoy receptor that inhibits beneficial cardioprotective effects of IL-33; such inhibition results in cardiac hypertrophy, myocardial fibrosis, and ventricular dysfunction. Measurement of soluble ST2 has utility for assessing heart failure severity and prognosis...
January 2018: Heart Failure Clinics
https://www.readbyqxmd.com/read/29147584/il-33-acts-to-express-schaffer-collateral-ca1-ltp-and-regulate-learning-and-memory-by-targeting-myd88
#3
Tomoyuki Nishizaki
Interleukin-33 (IL-33) is recognized to transmit a signal through a heterodimeric receptor complex ST2/interleukin-1 receptor accessory protein (IL-1RAcP) bearing activation of myeloid differentiation factor 88 (MyD88). High-frequency stimulation to the Schaffer collateral induced long-term potentiation (LTP) in the CA1 region of hippocampal slices from wild-type control mice. Schaffer collateral/CA1 LTP in IL-33-deficient mice was significantly suppressed, which was neutralized by application with IL-33. Similar suppression of the LTP was found with MyD88-deficient mice but not with ST2-deficient mice...
2017: Neural Plasticity
https://www.readbyqxmd.com/read/29146574/mast-cell-dependent-il-33-st2-signaling-is-protective-against-the-development-of-airway-hyperresponsiveness-in-a-house-dust-mite-mouse-model-of-asthma
#4
Anna Maria Zoltowska Nilsson, Ying Lei, Mikael Adner, Gunnar P Nilsson
Interleukin-33 (IL-33) and its receptor ST2 have been influentially associated to the pathophysiology of asthma. Due to the divergent roles of IL-33 in regulating mast cell functions, there is a need to further characterize IL-33/ST2-dependent mast cell responses and their significance in the context of asthma. This study aimed to investigate how IL-33/ST2-dependent mast cell responses contribute to the development of airway hyperresponsiveness (AHR) and airway inflammation in a mouse model of house dust mite (HDM) induced asthma...
November 16, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29133293/il-33-responsive-group-2-innate-lymphoid-cells-are-regulated-by-female-sex-hormones-in-the-uterus
#5
Kathleen Bartemes, Chien-Chang Chen, Koji Iijima, Li Drake, Hirohito Kita
Group 2 innate lymphoid cells (ILC2s) reside in multiple organs in the body, where they play roles in immunity, tissue homeostasis, and metabolic regulation. However, little is known about the regulatory mechanisms of ILC2s in different organs. Here, we identified ILC2s in the mouse uterus and found that they express cell surface molecules, including the IL-33 receptor, ST2, that are roughly comparable to those expressed by lung ILC2s. Both in vivo and in vitro treatment with IL-33 induced type 2 cytokine production in uterine ILC2s, suggesting that they respond to IL-33 in a manner similar to ILC2s in other organs...
November 13, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/29076792/targeting-il-33-st2-signaling-regulation-of-immune-function-and-analgesia
#6
Victor Fattori, Miriam S N Hohmann, Ana C Rossaneis, Marilia F Manchope, Jose C Alves-Filho, Thiago M Cunha, Fernando Q Cunha, Waldiceu A Verri
IL-33 signals through ST2 receptor and promotes inflammation by activating downstream pathways culminating in the production of pro-inflammatory mediators such as IL-1β, TNF-α, and IL-6 in an NF-κB-dependent manner. In fact, compelling evidence has demonstrated the importance of IL-33/ST2 in both innate and adaptive immune responses in diseases presenting pain as an important clinical symptom. Areas covered: IL-33 is a pleiotropic cytokine with varied immune functions. Dysregulation of this pathway has been described as a key step in varied immune responses...
November 5, 2017: Expert Opinion on Therapeutic Targets
https://www.readbyqxmd.com/read/29069643/-repair-treg-cells-in-tissue-injury
#7
Chaoqi Zhang, Lifeng Li, Kexin Feng, Daoyang Fan, Wenhua Xue, Jingli Lu
Studies in mice and humans have elucidated an important role for Tregs in promoting tissue repair and restoring tissue integrity. Emerging evidence has revealed that Tregs promoted wound healing and repair processes at multiple tissue sites, such as the heart, liver, kidney, muscle, lung, bone and central nervous system. The localization of repair Tregs in the lung, muscle and liver exhibited unique phenotypes and functions. Epidermal growth factor receptor, amphiregulin, CD73/CD39 and keratinocyte growth factor are important repair factors that are produced or expressed by repair Tregs; these factors coordinate with parenchymal cells to limit injury and promote repair...
October 25, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29045902/epidermal-growth-factor-receptor-expression-licenses-type-2-helper-t-cells-to-function-in-a-t-cell-receptor-independent-fashion
#8
Carlos M Minutti, Sebastian Drube, Natalie Blair, Christian Schwartz, Jame C McCrae, Andrew N McKenzie, Thomas Kamradt, Michal Mokry, Paul J Coffer, Maria Sibilia, Alice J Sijts, Padraic G Fallon, Rick M Maizels, Dietmar M Zaiss
Gastro-intestinal helminth infections trigger the release of interleukin-33 (IL-33), which induces type-2 helper T cells (Th2 cells) at the site of infection to produce IL-13, thereby contributing to host resistance in a T cell receptor (TCR)-independent manner. Here, we show that, as a prerequisite for IL-33-induced IL-13 secretion, Th2 cells required the expression of the epidermal growth factor receptor (EGFR) and of its ligand, amphiregulin, for the formation of a signaling complex between T1/ST2 (the IL-33R) and EGFR...
October 17, 2017: Immunity
https://www.readbyqxmd.com/read/29038366/specifically-differentiated-t-cell-subset-promotes-tumor-immunity-over-fatal-immunity
#9
Abdulraouf Ramadan, Brad Griesenauer, Djamilatou Adom, Reuben Kapur, Helmut Hanenberg, Chen Liu, Mark H Kaplan, Sophie Paczesny
Allogeneic immune cells, particularly T cells in donor grafts, recognize and eliminate leukemic cells via graft-versus-leukemia (GVL) reactivity, and transfer of these cells is often used for high-risk hematological malignancies, including acute myeloid leukemia. Unfortunately, these cells also attack host normal tissues through the often fatal graft-versus-host disease (GVHD). Full separation of GVL activity from GVHD has yet to be achieved. Here, we show that, in mice and humans, a population of interleukin-9 (IL-9)-producing T cells activated via the ST2-IL-33 pathway (T9IL-33 cells) increases GVL while decreasing GVHD through two opposing mechanisms: protection from fatal immunity by amphiregulin expression and augmentation of antileukemic activity compared with T9, T1, and unmanipulated T cells through CD8α expression...
October 16, 2017: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/29032512/il-33-signalling-in-liver-immune-cells-enhances-drug-induced-liver-injury-and-inflammation
#10
Maísa Mota Antunes, Alan Moreira Araújo, Ariane Barros Diniz, Rafaela Vaz Sousa Pereira, Débora Moreira Alvarenga, Bruna Araújo David, Renata Monti Rocha, Maria Alice Freitas Lopes, Sarah Cozzer Marchesi, Brenda Naemi Nakagaki, Érika Carvalho, Pedro Elias Marques, Bernhard Ryffel, Valérie Quesniaux, Rodrigo Guabiraba Brito, José Carlos Alves Filho, Denise Carmona Cara, Rafael Machado Rezende, Gustavo Batista Menezes
OBJECTIVE AND DESIGN: The aim of this study was to investigate the contribution of IL-33/ST2 axis in the onset and progression of acute liver injury using a mice model of drug-induced liver injury (DILI). MATERIAL AND TREATMENTS: DILI was induced by overdose administration of acetaminophen (APAP) by oral gavage in wild-type BALB/c, ST2-deficient mice and in different bone marrow chimeras. Neutrophils were depleted by anti-Ly6G and macrophages with clodronate liposomes (CLL)...
October 14, 2017: Inflammation Research: Official Journal of the European Histamine Research Society ... [et Al.]
https://www.readbyqxmd.com/read/28978698/stopping-inflammation-in-stroke-role-of-st2-il-33-signaling
#11
Antoine Drieu, Sara Martinez de Lizarrondo, Marina Rubio
No abstract text is available yet for this article.
October 4, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28974430/predictive-value-of-low-interleukin-33-in-critically-ill-patients
#12
Konstantin A Krychtiuk, Stefan Stojkovic, Max Lenz, Mira Brekalo, Kurt Huber, Johann Wojta, Gottfried Heinz, Svitlana Demyanets, Walter S Speidl
Patients admitted to a medical intensive care unit (ICU) are characterized by an activated immune system and exhibit a high mortality rate irrespective of the underlying cause of admission. Interleukin (IL)-33 has been shown to be protective in experimental sepsis models and it has been demonstrated that circulating levels of its "decoy" receptor soluble ST2 (sST2) are associated with outcome in critically ill patients. The aim of the present study was to investigate whether circulating IL-33 is associated with 30-day mortality in patients admitted to a medical ICU...
September 30, 2017: Cytokine
https://www.readbyqxmd.com/read/28960823/changes-in-inflammatory-mediators-as-a-result-of-intermittent-hypoxia-in-obstructive-sleep-apnea-syndrome
#13
Volkan Sozer, Müge Kutnu, Ersan Atahan, Buket Calıskaner Ozturk, Ergi Hysi, Cansu Cabuk, Benan Musellim, Gonul Simsek, Hafize Uzun
BACKGROUND: Inflammation plays an important role in obstructive sleep apnea syndrome (OSAS). The objective of this study was to investigate the relationship of serum C-reactive protein(CRP), pentraxin-3(PTX-3), procalcitonin(ProCT), interleukin-33(IL-33) and its soluble receptor ST2 (sST2) with the syndrome severity and to show theirs importance as biomarkers. METHODS: This study comprises a total of 84 identical (sex and age wise) cases. Full-night polysomnography was performed in each patient...
September 29, 2017: Clinical Respiratory Journal
https://www.readbyqxmd.com/read/28952069/anti-il-33-antibody-has-a-therapeutic-effect-in-an-atopic-dermatitis-murine-model-induced-by-2-4-dinitrochlorobenzene
#14
Ge Peng, Zhenzhen Mu, Lixia Cui, Pengyue Liu, Ying Wang, Wenqing Wu, Xiuping Han
IL-33 is a new member of the IL-1 family that plays a role in allergic disease. In this study, we evaluated the potential on the inhibition of atopic dermatitis (AD) of anti-mouse IL-33 antibody (αIL-33Ab) using 2, 4-dinitrochlorobenzene (DNCB)-induced AD mice model. We treated mice with αIL-33Ab via subcutaneous injection of each DNCB treatment 1 h later from day 1 to day 33 for 14 times. A control group received tacrolimus. Skin lesion and scratching behavior were compared. Ear thickness, dermatitis score, eosinophils and mast cells infiltration, and serum IgE levels were also analyzed...
September 26, 2017: Inflammation
https://www.readbyqxmd.com/read/28943296/il-33-exacerbates-liver-sterile-inflammation-by-amplifying-neutrophil-extracellular-trap-formation
#15
Hamza O Yazdani, Hui-Wei Chen, Samer Tohme, Sheng Tai, Dirk J van der Windt, Patricia Loughran, Brian R Rosborough, Vikas Sud, Donna Beer-Stolz, Heth R Turnquist, Allan Tsung, Hai Huang
BACKGROUND: Neutrophils and Liver sinusoidal endothelial cells (LSECs) both contribute to sterile inflammatory injury during ischemia/reperfusion (I/R), a well-known liver surgical stress. Interleukin-33 (IL-33) has been shown to drive neutrophil infiltration during inflammatory responses through its receptor ST2. We recently reported that infiltrating neutrophils form neutrophil extracellular traps (NETs), which exacerbate sterile inflammatory injury in liver I/R. Here, we sought to determine the role of IL-33 in NET formation during liver sterile inflammation...
September 21, 2017: Journal of Hepatology
https://www.readbyqxmd.com/read/28930661/il-1-family-cytokines-use-distinct-molecular-mechanisms-to-signal-through-their-shared-co-receptor
#16
Sebastian Günther, Daniel Deredge, Amanda L Bowers, Alessandra Luchini, Daniel A Bonsor, Robert Beadenkopf, Lance Liotta, Patrick L Wintrode, Eric J Sundberg
Within the interleukin 1 (IL-1) cytokine family, IL-1 receptor accessory protein (IL-1RAcP) is the co-receptor for eight receptor-cytokine pairs, including those involving cytokines IL-1β and IL-33. Unlike IL-1β, IL-33 does not have a signaling complex that includes both its cognate receptor, ST2, and the shared co-receptor IL-1RAcP, which we now present here. Although the IL-1β and IL-33 complexes shared structural features and engaged identical molecular surfaces of IL-1RAcP, these cytokines had starkly different strategies for co-receptor engagement and signal activation...
September 19, 2017: Immunity
https://www.readbyqxmd.com/read/28916390/il-33-receptor-st2-deficiency-attenuates-renal-ischaemia-reperfusion-injury-in-euglycaemic-but-not-streptozotocin-induced-hyperglycaemic-mice
#17
M Sehnine, M Ferhat, S Sena, J M Gombert, J M Goujon, A Thierry, G Touchard, T Hauet, A Herbelin, S Hadjadj
AIM: Kidney hypoxia can predispose to the development of acute and chronic renal failure in diabetes. Ischaemia-reperfusion injury (IRI) causes inflammation, and diabetes is known to exacerbate this inflammatory response in the kidney, whereas alarmin IL-33 could act as an innate immune mediator during kidney IRI. Thus, the present study examined the impact of genetic IL-33 receptor ST2 deficiency (ST2-/-) on renal IRI in euglycaemic and hyperglycaemic mice. METHODS: Hyperglycaemia was induced with streptozotocin (STZ) in adult male C57BL/6JRj wild-type (WT) mice and ST2-/- mice...
September 12, 2017: Diabetes & Metabolism
https://www.readbyqxmd.com/read/28881817/dectin-1-signaling-inhibits-osteoclastogenesis-via-il-33-induced-inhibition-of-nfatc1
#18
Xiaoqing Zhu, Yinghua Zhao, Yuxue Jiang, Tianxue Qin, Jintong Chen, Xiao Chu, Qing Yi, Sujun Gao, Siqing Wang
Abnormal osteoclast activation contributes to osteolytic bone diseases (OBDs). It was reported that curdlan, an agonist of dectin-1, inhibits osteoclastogenesis. However, the underlying mechanisms are not fully elucidated. In this study, we found that curdlan potently inhibited RANKL-induced osteoclast differentiation and the resultant bone resorption. Curdlan inhibited the expression of nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1), the key transcriptional factor for osteoclastogenesis. Notably, dectin-1 activation increased the expression of MafB, an inhibitor of NFATc1, and IL-33 in osteoclast precursors...
August 8, 2017: Oncotarget
https://www.readbyqxmd.com/read/28881679/mir-487b-mitigates-chronic-heart-failure-through-inhibition-of-the-il-33-st2-signaling-pathway
#19
En-Wei Wang, Xu-Sheng Jia, Chang-Wu Ruan, Zhi-Ru Ge
We investigated the effects of microRNA-587b (miR-487b) in a rat model of chronic heart failure (CHF). Wistar rats were assigned to 10 groups (n=8 per group). Expression of interleukin-33 (IL-33), somatostatin 2 (ST2), IL-6, and TNF-α was higher in the CHF group than the control group. In the CHF, negative control (NC) for si-IL-33, NC for miR-487b mimic, NC for miR-487b inhibitor, and miR-487b inhibitor + si IL-33 groups, as compared to the blank and sham groups: steroid binding protein (SBP), D binding protein (DBP), left ventricular systolic pressure (LVSP), ± dp/dtmax, and superoxide dismutase (SOD) were all lower; myocardial fibrosis, MDA, left ventricular end-diastolic pressure (LVEDP), myocardial apoptosis rate, IL-6, and TNF-α were all higher; levels of IL-33 and ST2 mRNA and protein were higher; and levels of miR-487b were lower...
August 1, 2017: Oncotarget
https://www.readbyqxmd.com/read/28878285/interleukin-33-promotes-inflammation-induced-lymphangiogenesis-via-st2-traf6-mediated-akt-enos-no-signalling-pathway
#20
Longhui Han, Minglian Zhang, Xu Liang, Xin Jia, Jinchen Jia, Miying Zhao, Yiming Fan
The interplay between inflammation and lymphangiogenesis is mediated by various cytokines. However, most of these molecules and their associated mechanism are yet to be defined. Here, we explored the role of IL-33 in modulating inflammation-induced lymphangiogenesis (ILA) and its underlying mechanisms using an ILA mouse model and a lymphatic endothelial cell (LEC) line. Our results show that IL-33 promoted the proliferation, migration and tube formation of LECs and ILA in vivo. The pro-lymphangiogenic activity of IL-33 was abolished by ST2 blockage...
September 6, 2017: Scientific Reports
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