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Dongjiao Wang, Sujun Gao, Jintong Chen, Yinghua Zhao, Yuxue Jiang, Xiao Chu, Xiaohua Wang, Ning Liu, Tianxue Qin, Qing Yi, Ying Yue, Siqing Wang
Interleukin-33 (IL-33) is a potent contributor to antiviral immune responses and antitumor immunity. We recently discovered that IL-33 is overexpressed in dectin-1-activated dendritic cells (DCs). However, mechanisms of dectin-1-induced IL-33 expression in DCs remain elusive. Curdlan, an agonist of dectin-1, was used to mature DCs in this study. We found that dectin-1-induced IL-33 expression in DCs relies on Syk and Raf-1 pathways. By using nuclear factor (NF)-κB inhibitors, we also found that dectin-1-induced IL-33 expression relies on NF-κB signaling...
March 14, 2018: Laboratory Investigation; a Journal of Technical Methods and Pathology
M R Khaitov, A R Gaisina, I P Shilovskiy, V V Smirnov, G V Ramenskaia, A A Nikonova, R M Khaitov
Interleukin-33 (IL-33) belongs to the IL-1 cytokine family and plays an important role in modulating immune system by inducing Th2 immune response via the ST2 membrane receptor. Epithelial cells are the major producers of IL-33. However, IL-33 is also secreted by other cells, e.g., bone marrow cells, dendritic cells, macrophages, and mast cells. IL-33 targets a broad range of cell types bearing the ST2 surface receptor. Many ST2-positive cells, such as Th2 cells, mast cells, basophils, and eosinophils, are involved in the development of allergic bronchial asthma (BA)...
January 2018: Biochemistry. Biokhimii︠a︡
Mohammad Faruq Abd Rachman Isnadi, Voon Kin Chin, Roslaini Abd Majid, Tze Yan Lee, Maizaton Atmadini Abdullah, Ramatu Bello Omenesa, Zaid Osamah Ibraheem, Rusliza Basir
Interleukin-33 (IL-33) is an IL-1 family member, which exhibits both pro- and anti-inflammatory properties solely based on the type of the disease itself. Generally, IL-33 is expressed by both endothelial and epithelial cells and mediates its function based on the interaction with various receptors, mainly with ST2 variants. IL-33 is a potent inducer for the Th2 immune response which includes defence mechanism in brain diseases. Thus, in this paper, we review the biological features of IL-33 and the critical roles of IL-33/ST2 pathway in selected neurological disorders including Alzheimer's disease, multiple sclerosis, and malaria infection to discuss the involvement of IL-33/ST2 pathway during these brain diseases and its potential as future immunotherapeutic agents or for intervention purposes...
2018: Mediators of Inflammation
Min Yang, Yuehua Feng, Cuihua Yue, Bin Xu, Lujun Chen, Jingting Jiang, Binfeng Lu, Yibei Zhu
OBJECTIVE: Lung cancer is one of the deadliest malignancies. The immune checkpoint-blockade (ICB) tumor therapy has led to striking improvement of long-term survival for some lung cancer patients. However, the response rate of immunotherapy is still low for lung cancer. Studying the tumor microenvironment (TME) should shed light on improvement of immunotherapy of lung cancer. Interleukin-33 (IL-33), an "alarmin" cytokine, has been implicated in tumor associated immune responses and inflammatory diseases of the lung...
2018: PloS One
Zhiping Yang, Xin Gao, Jingyu Wang, Longsheng Xu, Ying Zheng, Yufen Xu
Aim: Interleukin-33 (IL-33), belonging to IL-1 family cytokines, has been reported to participate in cancer growth and metastasis. The clinical values of IL-33 in lung cancer have been previously investigated. We aimed to elucidate the probable role of IL-33 in the migration and invasion of lung cancer cells. Methods: Cell migration and invasiveness were tested by Transwell assay. Western blotting analysis was performed to detect protein expression. Results: We found that IL-33 treatment in human lung A549 cells dose-dependently enhanced their migratory and invasive ability, accompanied by elevated expression of matrix metallo-proteinase (MMP) 2 and MMP9...
2018: OncoTargets and Therapy
Anastasia I Petra, Irene Tsilioni, Alexandra Taracanova, Alexandra Katsarou-Katsari, Theoharis C Theoharides
BACKGROUND: Cytokine interleukin (IL) 31 has emerged as an important component of allergic and inflammatory diseases associated with pruritus, such as atopic dermatitis (AD) and mastocytosis. Mast cells (MC) are stimulated by allergic and nonallergic triggers, and play a critical role in such diseases by secreting histamine and tryptase as well as cytokines and chemokines. IL-33 has been reported to augment MC responses, but its effect on secretion of IL-31 is not known. OBJECTIVES: To investigate whether IL-33 can stimulate the secretion of IL-31 from cultured human MCs and whether this response is augmented by either the neuropeptide substance P (SP) or immunoglobulin E (IgE) and anti-IgE in the absence or presence of IL-4...
March 1, 2018: Allergy and Asthma Proceedings:
Naina Gour, Stephane Lajoie, Ursula Smole, Marquitta White, Donglei Hu, Pagé Goddard, Scott Huntsman, Celeste Eng, Angel Mak, Sam Oh, Jung-Hyun Kim, Annu Sharma, Sophie Plante, Ikhlass Haj Salem, Yvonne Resch, Xiao Xiao, Nu Yao, Anju Singh, Susanne Vrtala, Jamila Chakir, Esteban G Burchard, Andrew P Lane, Marsha Wills-Karp
The key factors underlying the development of allergic diseases-the propensity for a minority of individuals to develop dysfunctional responses to harmless environmental molecules-remain undefined. We report a pathway of immune counter-regulation that suppresses the development of aeroallergy and shrimp-induced anaphylaxis. In mice, signaling through epithelially expressed dectin-1 suppresses the development of type 2 immune responses through inhibition of interleukin-33 (IL-33) secretion and the subsequent recruitment of IL-13-producing innate lymphoid cells...
February 23, 2018: Science Immunology
Ian C Scott, Jayesh B Majithiya, Caroline Sanden, Peter Thornton, Philip N Sanders, Tom Moore, Molly Guscott, Dominic J Corkill, Jonas S Erjefält, E Suzanne Cohen
Interleukin (IL)-33 is an IL-1 family alarmin released from damaged epithelial and endothelial barriers to elicit immune responses and allergic inflammation via its receptor ST2. Serine proteases released from neutrophils, mast cells and cytotoxic lymphocytes have been proposed to process the N-terminus of IL-33 to enhance its activity. Here we report that processing of full length IL-33 can occur in mice deficient in these immune cell protease activities. We sought alternative mechanisms for the proteolytic activation of IL-33 and discovered that exogenous allergen proteases and endogenous calpains, from damaged airway epithelial cells, can process full length IL-33 and increase its alarmin activity up to ~60-fold...
February 20, 2018: Scientific Reports
Moritz F Eissmann, Christine Dijkstra, Merridee A Wouters, David Baloyan, Dmitri Mouradov, Paul M Nguyen, Mercedes Davalos-Salas, Tracy L Putoczki, Oliver M Sieber, John M Mariadason, Matthias Ernst, Frederick Masson
Interleukin 33 (IL33) is an inflammatory cytokine released during necrotic cell death. The epithelium and stroma of the intestine express large amounts of IL33 and its receptor St2. IL33 is therefore continuously released during homeostatic turnover of the intestinal mucosa. Although IL33 can prevent colon cancer associated with inflammatory colitis, the contribution of IL33 signaling to sporadic colon cancer remains unknown. Here, we utilized a mouse model of sporadic colon cancer to investigate the contribution of IL33 signaling to tumorigenesis in the absence of pre-existing inflammation...
February 20, 2018: Cancer Immunology Research
Gao An, Xin Zhang, Wenjun Wang, Qiong Huang, Yan Li, Shan Shan, Chris J Corrigan, Wei Wang, Sun Ying
It has been suggested that interleukin 33 (IL-33) plays an important role in the pathogenesis of asthma through a variety of pathways, but its role in airways fibrosis in asthma has not been fully elucidated. In the present study we evaluated changes in the expression of extracellular matrix proteins (ECMs) as well as matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) in an IL-33-induced, antigen-independent murine surrogate of asthma as well as a conventional surrogate employing per-nasal challenge of mice previously sensitised to produce an IgE response to ovalbumin (OVA)...
February 18, 2018: Immunology
Qian Li, Dulei Li, Xian Zhang, Qingqing Wan, Wen Zhang, Mingke Zheng, Le Zou, Chris Elly, Jee H Lee, Yun-Cai Liu
Group 2 innate lymphoid cells (ILC2s) are a specialized subset of lymphoid effector cells that are critically involved in allergic responses; however, the mechanisms of their regulation remain unclear. We report that conditional deletion of the E3 ubiquitin ligase VHL in innate lymphoid progenitors minimally affected early-stage bone marrow ILC2s but caused a selective and intrinsic decrease in mature ILC2 numbers in peripheral non-lymphoid tissues, resulting in reduced type 2 immune responses. VHL deficiency caused the accumulation of hypoxia-inducible factor 1α (HIF1α) and attenuated interleukin-33 (IL-33) receptor ST2 expression, which was rectified by HIF1α ablation or inhibition...
February 6, 2018: Immunity
Ilia D Vainchtein, Gregory Chin, Frances S Cho, Kevin W Kelley, John G Miller, Elliott C Chien, Shane A Liddelow, Phi T Nguyen, Hiromi Nakao-Inoue, Leah C Dorman, Omar Akil, Satoru Joshita, Ben A Barres, Jeanne T Paz, Ari B Molofsky, Anna V Molofsky
Neuronal synapse formation and remodeling is essential to central nervous system (CNS) development and is dysfunctional in neurodevelopmental diseases. Innate immune signals regulate tissue remodeling in the periphery, but how this impacts CNS synapses is largely unknown. Here, we show that the IL-1 family cytokine interleukin-33 (IL-33) is produced by developing astrocytes and is developmentally required for normal synapse numbers and neural circuit function in the spinal cord and thalamus. We find that IL-33 signals primarily to microglia under physiologic conditions, that it promotes microglial synapse engulfment, and that it can drive microglial-dependent synapse depletion in vivo...
February 1, 2018: Science
Eisuke Dohi, Eric Y Choi, Indigo V L Rose, Akiho S Murata, Sharon Chow, Minae Niwa, Shin-Ichi Kano
Interleukin (IL)-33 is a member of the IL-1 family of cytokines. IL-33 is expressed in nuclei and secreted as alarmin upon cellular damage to deliver a danger signal to the surrounding cells. Previous studies showed that IL-33 is expressed in the brain and that it is involved in neuroinflammatory and neurodegenerative processes in both humans and rodents. Nevertheless, the role of IL-33 in physiological brain function and behavior remains unclear. Here, we have investigated the behaviors of mice lacking IL-33 (Il33-/- mice)...
November 2017: ENeuro
Katsuyuki Umebashi, Akinori Tokito, Masayoshi Yamamoto, Michihisa Jougasaki
Interleukin (IL)-33 is a member of the IL-1 cytokine family with dual functions as a traditional cytokine and as a transcriptional regulator. We recently reported that IL-33 up-regulated growth regulated oncogene (GRO)-α/CXCL1 expression in human vascular endothelial cells. The aim of this study was to investigate the effect of IL-33 on the expression of IL-8/CXCL8, another member of the CXC-chemokine family, and to elucidate its signaling pathways in human umbilical vein endothelial cells (HUVECs). Immunocytochemical staining and Western immunoblot analysis revealed that IL-33 augmented IL-8 protein expression in HUVECs...
2018: PloS One
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
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
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
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
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
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
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