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Mehmet Rafet Yigitbasi, Gulcan Guntas, Tuba Atak, Cigdem Sonmez, Haydar Yalman, Hafize Uzun
INTRODUCTION: Idiopathic granulomatous mastitis (IGM) is a rare benign inflammatory breast disease that can clinically and radiographically mimic breast carcinoma and bacterial mastitis. The aim of this study is to investigate the importance of levels of the inflammation markers, interleukin-33 (IL-33), soluble ST2 receptor of IL-33 (sST2), procalcitonin (PCT), and CRP on differential diagnosis of IGM and breast cancer (BC). METHODS: 25 patients with IGM and 32 patients with primary BC who applied to General Surgery Clinic, and 30 healthy volunteer women with similar demographic condition were enrolled in the study...
October 26, 2016: Journal of Investigative Surgery: the Official Journal of the Academy of Surgical Research
Hideaki Kouzaki, Koji Matsumoto, Hirotaka Kikuoka, Tomohisa Kato, Ichiro Tojima, Shino Shimizu, Hirohito Kita, Takeshi Shimizu
RATIONALE: Cystatin A and SPINK5 are endogenous protease inhibitors (EPIs) that may play key roles in epithelial barrier function. OBJECTIVE: The purpose of this study was to investigate the roles of EPIs in the pathogenesis of chronic rhinosinusitis (CRS). METHODS: We examined the expression of cystatin A and SPINK5 in the nasal epithelial cells of patients with CRS. Additionally, the in vitro effects of recombinant EPIs on the secretion of the epithelial-derived cytokines, interleukin (IL)-25, IL-33 and thymic stromal lymphopoietin (TSLP), in airway epithelial cells, and the in vivo effects of recombinant EPIs in the nasal epithelium of mice exposed to multiple airborne allergens (MAA) were examined...
October 25, 2016: American Journal of Respiratory and Critical Care Medicine
Hajime Ishinaga, Masako Kitano, Masaaki Toda, Corina N D'Alessandro-Gabazza, Esteban C Gabazza, Said Ahmad Shah, Kazuhiko Takeuchi
We investigated whether IL-33 is involved in mucus overproduction and goblet cell hyperplasia in eosinophilic chronic rhinosinusitis (ECRS). IL-33 mRNA was significantly higher in the eosinophilic CRS group than in the non-eosinophilic CRS group from human nasal polyps. IL-33 induced MUC5AC mRNA and MUC5AC protein, and also goblet cell hyperplasia at air liquid interface culture in human nasal epithelial cells. In addition to that, IL-33 induced MUC5B and FOXA3, and reduces FOXJmRNA. In conclusion, our present study demonstrated that the direct evidence of IL-33 which lead to increase mucin gene and protein expression, as well as goblet cell hyperplasia...
October 21, 2016: Cytokine
Ankit Malik, Deepika Sharma, Qifan Zhu, Rajendra Karki, Clifford S Guy, Peter Vogel, Thirumala-Devi Kanneganti
Inflammatory bowel diseases (IBD) affect over 5 million individuals in the industrialized world, with an increasing incidence rate worldwide. IBD also predisposes affected individuals to development of colorectal cancer, which is a leading cause of cancer-related deaths in adults. Mutations in genes encoding molecules in the IL-33 signaling pathway are associated with colitis and colitis-associated cancer (CAC), but how IL-33 modulates gut homeostasis is unclear. Here, we have shown that Il33-deficient mice are highly susceptible to colitis and CAC...
October 24, 2016: Journal of Clinical Investigation
Monika Ryba-Stanisławowska, Paulina Werner, Maria Skrzypkowska, Agnieszka Brandt, Jolanta Myśliwska
IL-33 is an IL-1 cytokine family member, with ability to induce both Th1 and Th2 immune responses. It binds to ST2 receptor, whose deficiency is associated with enhanced inflammatory response. The most recent studies have shown the immunoregulatory effect of IL-33 on Tregs in animal models. As type 1 diabetes is an autoimmune, inflammatory disease, where Treg defects have been described, we aimed to analyze the in vitro influence of recombinant IL-33 on quantitative properties of regulatory CD4(+)CD25(high)FOXP3(+) T cells...
2016: Mediators of Inflammation
Steven J Van Dyken, Jesse C Nussbaum, Jinwoo Lee, Ari B Molofsky, Hong-Erh Liang, Joshua L Pollack, Rachel E Gate, Genevieve E Haliburton, Chun J Ye, Alexander Marson, David J Erle, Richard M Locksley
Group 2 innate lymphoid cells (ILC2s) and CD4(+) type 2 helper T cells (TH2 cells) are defined by their similar effector cytokines, which together mediate the features of allergic immunity. We found that tissue ILC2s and TH2 cells differentiated independently but shared overlapping effector function programs that were mediated by exposure to the tissue-derived cytokines interleukin 25 (IL-25), IL-33 and thymic stromal lymphopoietin (TSLP). Loss of these three tissue signals did not affect lymph node priming, but abrogated the terminal differentiation of effector TH2 cells and adaptive lung inflammation in a T cell-intrinsic manner...
October 17, 2016: Nature Immunology
Xu Shi, Ying Tang, Xiguang Sun, Yufei Liu, Ying Sun, Munan Sun, Yanfang Jiang, Yulin Li
The current study aimed to investigate the distribution of memory and naïve T cell (TN) subsets in hepatitis B virus (HBV)‑infected patients at different immune stages and investigate the effect of interleukin 33 (IL‑33) on the regulation of the T‑cell subsets. The distributions of memory and naïve T cells were detected by flow cytometry. ELISA was conducted to assess the levels of IL‑4, IL‑5, IL‑10, IL‑12, interferon γ and tumor necrosis factor α. The expression levels of IL‑33 and HBV x protein (HBx) were measured by reverse transcription‑quantitative polymerase chain reaction and western blot analysis, respectively...
October 13, 2016: Molecular Medicine Reports
Jinggang Xia, Yang Qu, Chunlin Yin, Dong Xu
BACKGROUND: This study aimed to evaluate the role of β-blocker therapy on modulating interleukin (IL)-33/ST2 (interleukin-1 receptor-like 1) signaling during ventricular remodeling related to heart failure (HF) after acute myocardial infarction (AMI). METHODS: Sprague-Dawley rats that survived surgery to induce AMI were randomly divided into the placebo group and the β-blocker treatment group. A sham group was used as a control. Left ventricular (LV) function variables, the myocardial infarct size, fibrosis and IL-33/ST2 protein expression was measured...
October 17, 2016: Cardiology Journal
Mona Dixon Gundersen, Rasmus Goll, Johanna Hol, Trine Olsen, Renathe Rismo, Sveinung W Sørbye, Olav Sundnes, Guttorm Haraldsen, Jon Florholmen
Interleukin 33 (IL-33) is a cytokine preferentially elevated in acute ulcerative colitis (UC), inferring a role in its pathogenesis. The role of IL-33 in intestinal inflammation is incompletely understood, with both pro-inflammatory and regulatory properties described. There are also conflicting reports on cellular sources and subcellular location of IL-33 in the colonic mucosa, justifying a closer look at IL-33 expression in well-defined clinical stages of UC. A total of 50 study participants (29 UC patients and 21 healthy controls) were included from a prospective cohort of inflammatory bowel disease patients treated to disease remission with infliximab, a tumour necrosis factor alpha (TNF) inhibitor...
October 17, 2016: Scientific Reports
Magdalena Paplińska-Goryca, Patrycja Nejman-Gryz, Katarzyna Górska, Katarzyna Białek-Gosk, Joanna Hermanowicz-Salamon, Rafał Krenke
Asthma and COPD are the most common obstructive lung diseases characterized by inflammation in the lower airways which contribute to airflow limitation. Different inflammatory mediators are thought to play a key role in these diseases. This study was conducted in 13 patients with asthma, 12 patients with COPD, and 13 control subjects. The expression of mRNA of IL-6, IL-13, CXCL8, TSLP, IL-33, IL-25, IL-17, ECP, mast cell tryptase, CCL24, and CCL26 was assessed in induced sputum cells by real time PCR. We found that CXCL8 was strongly related to the neutrophil percentage but differed significantly in COPD and asthma patients...
October 14, 2016: Advances in Experimental Medicine and Biology
Amir S Yazdi, Kamran Ghoreschi
The interleukin-1 (IL-1) family consists of several pro- or anti-inflammatory proteins, with pro-inflammatory IL-1β being its best characterized member. IL-1β is one of the most prominent mediators of inflammation resulting in fever and immune activation via binding to IL-1 receptor 1. Due to its potency, its secretion is tightly regulated. First the transcription of the biologically inactive proform is induced by TLR activation, TNF, or IL-1 receptor activation by mature IL-1α or IL-1β. For the secretion of IL-1β, inflammasome activation as second stimulus is needed...
2016: Advances in Experimental Medicine and Biology
Meriam Nefla, Dirk Holzinger, Francis Berenbaum, Claire Jacques
Alarmins (also known as danger signals) are endogenous molecules that are released to the extracellular milieu after infection or tissue damage. Extracellular alarmins interact with specific receptors expressed by cells that are engaged in host defence to stimulate signalling pathways that result in initiation of innate and adaptive immune responses, triggering inflammation or tissue repair. Alarmins are considered to be markers of destructive processes that occur in degenerative joint diseases (primarily osteoarthritis (OA)) and chronic inflammatory joint diseases (such as rheumatoid arthritis, psoriatic arthritis and spondylarthropathy)...
October 13, 2016: Nature Reviews. Rheumatology
Man K S Lee, Laurent Yvan-Charvet, Seth L Masters, Andrew J Murphy
Obesity is now recognised as a chronic, low-grade inflammatory disease contributing to insulin resistance, type 2 diabetes (T2D) and cardiovascular disease (CVD). Multiple mechanisms leading to the low grade inflammation in this setting have been suggested. Due to the complexity and interconnection of inflammatory and metabolic responses, there also remains a need to fully elucidate the inflammatory mechanisms that control obesity and associated metabolic disorders. One important avenue in the field that has gained great attention is the interleukin (IL)-1 superfamily of cytokines that consist of IL-1β, IL-18 and IL-33...
October 7, 2016: Seminars in Immunology
Diamanda Rigas, Gavin Lewis, Jennifer L Aron, Bowen Wang, Homayon Banie, Ishwarya Sankaranarayanan, Lauriane Galle-Treger, Hadi Maazi, Richard Lo, Gordon J Freeman, Arlene H Sharpe, Pejman Soroosh, Omid Akbari
BACKGROUND: Atopic diseases including asthma exacerbate type 2 immune responses and involve a number of immune cell types, including regulatory T cells (Tregs) and the emerging group 2 innate lymphoid cells (ILC2s). While ILC2s are potent producers of type 2 cytokines, the regulation of ILC2 activation and function is not well understood. OBJECTIVE: In the present study, we evaluate for the first time how Tregs interact with pulmonary ILC2s and control their function...
October 4, 2016: Journal of Allergy and Clinical Immunology
Lianshuang Zhang, Jialiu Wei, Lihua Ren, Jin Zhang, Man Yang, Li Jing, Ji Wang, Zhiwei Sun, Xianqing Zhou
Endosulfan, an organochlorine pesticide, was found in human blood, and its possible cardiovascular toxicity has been suggested. However, the mechanism about endothelial cell injuries induced by endosulfan has remained unknown. In the present study, human umbilical vein endothelial cells (HUVECs) were chosen to explore the toxicity mechanism and were treated with 0, 1, 6, and 12 μg/mL(-1) endosulfan for 24 h, respectively. The results showed that exposure to endosulfan could inhibit the cell viability, increase the release of lactate dehydrogenase (LDH), damage the ultrastructure, and lead to apoptosis and necroptosis in HUVECs...
October 5, 2016: Environmental Science and Pollution Research International
Carl D Richards, Laura Izakelian, Anisha Dubey, Grace Zhang, Steven Wong, Karen Kwofie, Aatif Qureshi, Fernando Botelho
IL-33 modulates both innate and adaptive immune responses at tissue sites including lung and may play critical roles in inflammatory lung disease. Although IL-33 expression can be altered upon NF-Kappa B activation, here we examine regulation by Oncostatin M, a gp130 cytokine family member, in mouse lung tissue. Responses were assessed in BALB/c mouse lung at day 7 of transient overexpression using endotracheally administered adenovirus encoding OSM (AdOSM) or empty vector (AdDel70). Whole lung extracts showed induction of IL-33 mRNA (>20-fold) and protein (10-fold increase in immunoblots) by AdOSM relative to AdDel70...
2016: Mediators of Inflammation
Sofia Theodoropoulou, David A Copland, Jian Liu, Jiahui Wu, Peter J Gardner, Ema Ozaki, Sarah L Doyle, Matthew Campbell, Andrew D Dick
Age-related macular degeneration (AMD) is the leading cause of central vision loss worldwide. Loss of retinal pigment epithelium (RPE) is a major pathological hallmark in AMD with or without pathological neovascularization. Although activation of the immune system is implicated in disease progression, pathological pathways remain diverse and unclear. Here, we report an unexpected protective role of a pro-inflammatory cytokine, interleukin-33 (IL-33) in ocular angiogenesis. IL-33 and its receptor (ST2) are expressed constitutively in human and murine retina and choroid...
October 4, 2016: Journal of Pathology
Erin D Gordon, Joe Palandra, Agata Wesolowska-Andersen, Lando Ringel, Cydney L Rios, Marrah E Lachowicz-Scroggins, Louis Z Sharp, Jamie L Everman, Hannah J MacLeod, Jae W Lee, Robert J Mason, Michael A Matthay, Richard T Sheldon, Michael C Peters, Karl H Nocka, John V Fahy, Max A Seibold
Genome-wide association studies of asthma have identified genetic variants in the IL1RL1 gene, but the molecular mechanisms conferring risk are unknown. IL1RL1 encodes the ST2 receptor (ST2L) for IL-33 and an inhibitory decoy receptor (sST2). IL-33 promotes type 2 inflammation, which is present in some but not all asthmatics. We find that two single nucleotide polymorphisms (SNPs) in IL1RL1 - rs1420101 and rs11685480 - are strongly associated with plasma sST2 levels, though neither is an expression quantitative trait locus (eQTL) in whole blood...
September 8, 2016: JCI Insight
Li Qian, Lin Yuanshao, Huang Wensi, Zhou Yulei, Chen Xiaoli, Wang Brian, Zhang Wanli, Cai Zhengyi, Xue Jie, Zhang Wenhui, Yu Tieer, Wang Hong, He Jincai, Jin Kunlin, Shao Bei
Interleukin-33 (IL-33), a newly recognized IL-1 family member, is expressed in various tissues and cells, and involved in pathogenesis of many human diseases. For example, IL-33 plays a protective role in cardiovascular diseases. However, the role of IL-33 in acute ischemic stroke (AIS) remains unclear. This study aims to investigate whether IL-33 level in AIS patient serum can be used as a potential diagnostic and prognostic marker. The study included two hundred and six patients with first-ever ischemic stroke, who were admitted within 72 hours after stroke onset...
October 2016: Aging and Disease
Jiexiu Zhang, Zijie Wang, Zhen Xu, Zhijian Han, Jun Tao, Pei Lu, Zhengkai Huang, Wanli Zhou, Chunchun Zhao, Ruoyun Tan, Min Gu
BACKGROUND Chronic allograft dysfunction (CAD) is the major factor endangering the long-term allograft survival in kidney transplantation. The mechanisms of CAD remain unclear. MATERIAL AND METHODS A total of 64 renal transplant recipients were enrolled in our study and divided into a stable group and CAD group according to their allograft function. A group of 32 normal controls (healthy volunteers) were also included. An ELISA was used to detect serum interleukin-33 (IL-33), IL-2, IL-4, IL-10, IL-17, and interferon-gamma (IFN-γ)...
October 4, 2016: Annals of Transplantation: Quarterly of the Polish Transplantation Society
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