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https://www.readbyqxmd.com/read/28526653/genetic-variants-of-interleukin-18-are-associated-with-reduced-risk-of-atrial-fibrillation-in-a-population-from-northeast-china
#1
Ying-Hui Wang, Lin Fu, Bo Wang, Shu-Feng Li, Zhao Sun, Ying Luan
Atrial fibrillation (AF) affects approximately 1-2% of general population. Chronic inflammation plays an important role in AF development and interleukin-18 (IL-18) is a pro-inflammatory cytokine. This study aimed to assess the association of single nucleotide polymorphisms (SNPs) of IL-18 for with AF risk. Blood samples were taken from 243 AF patients and 160 non-AF individuals from a Chinese population and subjected to genotyping for six IL-18 SNPs using the MassArray system. Association of individual SNPs with AF risk was analyzed using SAS version 9...
May 16, 2017: Gene
https://www.readbyqxmd.com/read/28526582/mait-cells-a-tailor-made-mate-in-the-ancient-battle-against-infectious-diseases
#2
REVIEW
Marcela de Lima Moreira, Moriya Tsuji, Alexandra Jane Corbett, Márcio Sobreira Silva Araújo, Andréa Teixeira-Carvalho, Olindo Assis Martins-Filho, Vanessa Peruhype-Magalhães, Jordana Grazziela Coelho-Dos-Reis
It has been almost two decades since the discovery of mucosal-associated invariant T (MAIT)-cells. Several advances in the field have been made such as the discovery of the antimicrobial activity of MAIT-cells, the abundance of these cells in human mucosa and in liver and the discovery of ligands able to bind MR1 and activate MAIT-cells. MAIT-cells are a unique subset of innate-like T-cells that express a canonical T-cell receptor with the alpha chain containing hAV7S2 and AJ33 in humans (TCRVα7.2Jα33) and respond to bacterial/fungus vitamin B2 metabolites by an MR1-dependent pathway...
May 16, 2017: Immunology Letters
https://www.readbyqxmd.com/read/28526544/interleukin-18-gene-deletion-protects-against-sepsis-induced-cardiac-dysfunction-by-inhibiting-pp2a-activity
#3
Yoshitaka Okuhara, Shunichi Yokoe, Toshihiro Iwasaku, Akiyo Eguchi, Koichi Nishimura, Wen Li, Makiko Oboshi, Yoshiro Naito, Toshiaki Mano, Michio Asahi, Haruki Okamura, Tohru Masuyama, Shinichi Hirotani
BACKGROUND: Interleukin-18 (IL-18) neutralization protects against lipopolysaccharide (LPS)-induced injuries, including myocardial dysfunction. However, the mechanism is yet to be fully elucidated. The aim of the present study was to determine whether IL-18 gene deletion prevents sepsis-induced cardiac dysfunction and to elucidate the potential mechanisms underlying IL-18-mediated cardiotoxicity by LPS. METHODS AND RESULTS: Ten-week-old male wild-type (WT) and IL-18 knockout (IL-18 KO) mice were intraperitoneally administered LPS...
May 4, 2017: International Journal of Cardiology
https://www.readbyqxmd.com/read/28525945/the-protective-effect-of-luteolin-on-myocardial-ischemia-reperfusion-i-r-injury-through-tlr4-nf-%C3%AE%C2%BAb-nlrp3-inflammasome-pathway
#4
Xu Zhang, Qianming Du, Yan Yang, Jianing Wang, Shuai Dou, Chao Liu, Junguo Duan
The purpose of the present study was to investigate the effect of Luteolin(Lut) on myocardial ischemia reperfusion injury and explore the underlying mechanism. Myocardial ischemia reperfusion injury (I/R) model was induced with 30min of left anterior descending (LAD) occlusion followed by 24h of reperfusion. In vivo, the rats were randomly divided into 5 groups: (1)Sham, (2)I/R, (3)I/R+Lut(40mg/kg), (4)I/R+Lut(80mg/kg) and (5)I/R+Lut(160mg/kg). In vitro, the H9c2 cells were assigned to five groups: (1)control, (2)hypoxia-reoxygenation(H/R), (3)H/R+Lut(5μM), (4)H/R+Lut(10μM) and (5)H/R+Lut(20μM)...
May 15, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28521284/cytokine-mediated-activation-of-human-ex-vivo-expanded-v%C3%AE-9v%C3%AE-2-t-cells
#5
Eisuke Domae, Yuya Hirai, Takashi Ikeo, Seiji Goda, Yoji Shimizu
Vγ9Vδ2 T cells, the major subset of the human peripheral blood γδ T-cell, respond to microbial infection and stressed cells through the recognition of phosphoantigens. In contrast to the growing knowledge of antigen-mediated activation mechanisms, the antigen-independent and cytokine-mediated activation mechanisms of Vγ9Vδ2 T cells are poorly understood. Here, we show that interleukin (IL) -12 and IL-18 synergize to activate human ex vivo-expanded Vγ9Vδ2 T cells. Vγ9Vδ2 T cells treated with IL-12 and IL-18 enhanced effector functions, including the expression of IFN-γ and granzyme B, and cytotoxicity...
April 28, 2017: Oncotarget
https://www.readbyqxmd.com/read/28516117/reconstruction-of-the-mouse-inflammasome-system-in-hek293t-cells
#6
Hexin Shi, Anne Murray, Bruce Beutler
The NLRP3 (NLR family, Pyrin domain containing 3) inflammasome is a multiprotein complex comprised of NLRP3, pro-caspase-1, the adaptor protein apoptosis-associated speck-like protein containing a CARD (ASC), and the protein kinase NIMA related kinase 7 (NEK7) (Shi et al., 2016; He et al., 2016; Schmid-Burgk et al., 2016). When cells are exposed to microbes and/or danger signals, the inflammasome assembles and serves as a platform for the activation of caspase-1. Caspase-1 activation promotes the processing and secretion of the pro-inflammatory cytokines interleukin-1β (IL-1β), IL-18, and IL-33 as well as pyroptosis induction (Gross et al...
November 5, 2016: Bio-protocol
https://www.readbyqxmd.com/read/28516116/asc-particle-induced-peritonitis
#7
Lucia de Almeida, Andrea Dorfleutner, Christian Stehlik
In response to pathogen infection and tissue damage, inflammasome sensors such as NLRP3 and AIM2 are activated, which triggers PYRIN domain (PYD)-mediated ASC nucleation, followed by self-perpetuating ASC polymerization, which ultimately culminates in caspase-1 activation, interleukin (IL)-1β and IL-18 processing and release and pyroptosis (Ratsimandresy et al., 2013; Cai et al., 2014). Inflammasomes release not only cytokines, but also the polymeric ASC danger particles (pASC) by pyroptosis, which perpetuate and propagate inflammasome responses to bystander cells to engage cell intrinsic ASC and caspase-1 (Baroja-Mazo et al...
October 5, 2016: Bio-protocol
https://www.readbyqxmd.com/read/28515387/functional-polymorphisms-affecting-th1-differentiation-are-associated-with-the-severity-of-autoimmune-thyroid-diseases
#8
Naoya Inoue, Mikio Watanabe, Azusa Nakaguchi, Daishi Ueda, Hayaka Kawaguti, Yoh Hidaka, Yoshinori Iwatani
The prognosis for autoimmune thyroid diseases (AITDs), such as Hashimoto's disease (HD) and Graves' disease (GD), varies among patients. Interleukin (IL)-12 and IL-18 also induce Th1 differentiation, and SOCS1 (Suppressor of cytokine signaling 1) and TIM-3 (T cell immunoglobulin and mucin domain-3) are known to be negative regulators of Th1 cells. To clarify the association of functional polymorphisms in the IL12, IL12Rβ1, IL18, SOCS1 and TIM3 genes with the intractability and severity of autoimmune thyroid disease (AITD), we genotyped these polymorphisms in 151 GD patients, including 61 patients with intractable GD and 51 patients with GD in remission, in 140 HD patients, including 59 patients with severe HD and 55 patients with mild HD, and in 74 healthy controls...
May 16, 2017: Endocrine Journal
https://www.readbyqxmd.com/read/28508444/increased-adipose-tissue-expression-of-il-18r-and-its-ligand-il-18-associates-with-inflammation-and-insulin-resistance-in-obesity
#9
Rasheed Ahmad, Reeby Thomas, Shihab Kochumon, Sardar Sindhu
INTRODUCTION: The proinflammatory cytokine IL-18 is involved in the pathogenesis of metabolic syndrome. While the changes in IL-18 are known, IL-18R expression and relationship with IL-18 and other inflammatory markers in the adipose tissue in obesity/type-2 diabetes (T2D) remain unclear. METHODS: We, therefore, determined the adipose tissue expression of IL-18R and IL-18 mRNA/protein in lean, overweight, and obese individuals with and without T2D, 15 each, using qRT-PCR, immunohistochemistry, and confocal microscopy...
May 15, 2017: Immunity, Inflammation and Disease
https://www.readbyqxmd.com/read/28507179/elevated-expression-of-the-nlrp3-inflammasome-and-its-correlation-with-disease-activity-in-adult-onset-still-disease
#10
Chia-Wei Hsieh, Yi-Ming Chen, Chi-Chen Lin, Kuo-Tung Tang, Hsin-Hua Chen, Wei-Ting Hung, Kuo-Lung Lai, Der-Yuan Chen
OBJECTIVE: The dysregulation of the NLRP3 (NLR containing a pyrin domain) inflammasome is involved in autoinflammatory diseases. Adult-onset Still disease (AOSD) is regarded as an autoinflammatory disease. However, the pathogenic involvement of NLRP3 inflammasome in AOSD remains unclear and NLRP3 activators in AOSD are currently unknown. METHODS: The mRNA expression of NLRP3 inflammasome signaling in peripheral blood mononuclear cells (PBMC) from 34 patients with AOSD and 14 healthy subjects was determined using quantitative-PCR (qPCR)...
May 15, 2017: Journal of Rheumatology
https://www.readbyqxmd.com/read/28503820/the-p2x7-receptor-nlrp3-inflammasome-complex-predicts-the-development-of-non-hodgkin-s-lymphoma-in-sjogren-s-syndrome-a-prospective-observational-single-center-study
#11
Chiara Baldini, Eleonora Santini, Chiara Rossi, Valentina Donati, Anna Solini
BACKGROUND: P2X7 receptor (P2X7R), trigger of acute inflammatory responses via the NLRP3 inflammasome, is hyperfunctioning in patients with Sjogren Syndrome (SS), where it stimulates IL-18 production. Some patients with SS develop a mucosa-associated lymphoid tissue non-Hodgkin's lymphoma (MALT-NHL). OBJECTIVES: To prospectively evaluate the involvement and the putative prognostic role of this inflammatory pathway in the development of MALT-NHL. METHODS: 147 women with SS have been prospectively followed for a mean of 52 months, relating the expression and function of the P2X7R-inflammasome axis in salivary glands and circulating lymphomonocytes to the prognosis and the degree of the disease...
May 15, 2017: Journal of Internal Medicine
https://www.readbyqxmd.com/read/28494866/epithelial-histone-deacetylase-3-instructs-intestinal-immunity-by-coordinating-local-lymphocyte-activation
#12
Nazanin Navabi, Jordan Whitt, Shu-En Wu, Vivienne Woo, Jessica Moncivaiz, Michael B Jordan, Bruce A Vallance, Sing Sing Way, Theresa Alenghat
Mucosal tissues are constantly in direct contact with diverse beneficial and pathogenic microbes, highlighting the need for orchestrating complex microbial signals to sustain effective host defense. Here, we show an essential role for intestinal epithelial cell expression of histone deacetylase 3 (HDAC3) in responding to pathogenic microbes and activating protective innate immunity. Mice lacking HDAC3 in intestinal epithelial cells were more susceptible to Citrobacter rodentium when under tonic stimulation by the commensal microbiota...
May 9, 2017: Cell Reports
https://www.readbyqxmd.com/read/28492230/targeting-the-deubiquitinase-stambp-inhibits-nalp7-inflammasome-activity
#13
Joseph S Bednash, Nathaniel Weathington, James Londino, Mauricio Rojas, Dexter L Gulick, Robert Fort, SeungHye Han, Alison C McKelvey, Bill B Chen, Rama K Mallampalli
Inflammasomes regulate innate immune responses by facilitating maturation of inflammatory cytokines, interleukin (IL)-1β and IL-18. NACHT, LRR and PYD domains-containing protein 7 (NALP7) is one inflammasome constituent, but little is known about its cellular handling. Here we show a mechanism for NALP7 protein stabilization and activation of the inflammasome by Toll-like receptor (TLR) agonism with bacterial lipopolysaccharide (LPS) and the synthetic acylated lipopeptide Pam3CSK4. NALP7 is constitutively ubiquitinated and recruited to the endolysosome for degradation...
May 11, 2017: Nature Communications
https://www.readbyqxmd.com/read/28491822/comparison-of-the-expression-changes-after-botulinum-toxin-type-a-and-minocycline-administration-in-lipopolysaccharide-stimulated-rat-microglial-and-astroglial-cultures
#14
Anna Piotrowska, Katarzyna Popiolek-Barczyk, Flaminia Pavone, Joanna Mika
Botulinum neurotoxin type A (BoNT/A) and minocycline are potent drugs used in clinical therapies. The primary molecular mechanism of BoNT/A is the cleavage of SNARE proteins, which prevents cells from releasing neurotransmitters from vesicles, while the effects of minocycline are related to the inhibition of p38 activation. Both BoNT/A and minocycline exhibit analgesic effects, however, their direct impact on glial cells is not fully known. Therefore, the aim of the present study was to determine the effects of those drugs on microglial and astroglial activity after lipopolysaccharide (LPS) stimulation and their potential synergistic action...
2017: Frontiers in Cellular and Infection Microbiology
https://www.readbyqxmd.com/read/28491060/shaping-of-natural-killer-cell-antitumor-activity-by-ex-vivo-cultivation
#15
REVIEW
Markus Granzin, Juliane Wagner, Ulrike Köhl, Adelheid Cerwenka, Volker Huppert, Evelyn Ullrich
Natural killer (NK) cells are a promising tool for the use in adoptive immunotherapy, since they efficiently recognize and kill tumor cells. In this context, ex vivo cultivation is an attractive option to increase NK cells in numbers and to improve their antitumor potential prior to clinical applications. Consequently, various strategies to generate NK cells for adoptive immunotherapy have been developed. Here, we give an overview of different NK cell cultivation approaches and their impact on shaping the NK cell antitumor activity...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28489580/rapamycin-regulates-macrophage-activation-by-inhibiting-nlrp3-inflammasome-p38-mapk-nf%C3%AE%C2%BAb-pathways-in-autophagy-and-p62-dependent-manners
#16
Jung Hwa Ko, Sun-Ok Yoon, Hyun Ju Lee, Joo Youn Oh
Excessive and prolonged activation of macrophages underlies many inflammatory and autoimmune diseases. To regulate activation and maintain homeostasis, macrophages have multiple intrinsic mechanisms, one of which is modulation through autophagy. Here we demonstrate that autophagy induction by rapamycin suppressed the production of IL-1β and IL-18 in lipopolysaccharide- and adenosine triphosphate-activated macrophages at the post-transcriptional level by eliminating mitochondrial ROS (mtROS) and pro-IL1β in a p62/SQSTM1-dependent manner...
April 19, 2017: Oncotarget
https://www.readbyqxmd.com/read/28486971/a-role-for-cathepsin-z-in-neuroinflammation-provides-mechanistic-support-for-an-epigenetic-risk-factor-in-multiple-sclerosis
#17
Euan R O Allan, Rhiannon I Campden, Benjamin W Ewanchuk, Pankaj Tailor, Dale R Balce, Neil T McKenna, Catherine J Greene, Amy L Warren, Thomas Reinheckel, Robin M Yates
BACKGROUND: Hypomethylation of the cathepsin Z locus has been proposed as an epigenetic risk factor for multiple sclerosis (MS). Cathepsin Z is a unique lysosomal cysteine cathepsin expressed primarily by antigen presenting cells. While cathepsin Z expression has been associated with neuroinflammatory disorders, a role for cathepsin Z in mediating neuroinflammation has not been previously established. METHODS: Experimental autoimmune encephalomyelitis (EAE) was induced in both wildtype mice and mice deficient in cathepsin Z...
May 10, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28486793/inflammatory-bowel-disease-updates-on-molecular-targets-for-biologics
#18
REVIEW
Konstantinos H Katsanos, Konstantinos A Papadakis
Therapy for inflammatory bowel disease (IBD) has changed, with several new agents being evaluated. The era of anti-tumor necrosis factor (anti-TNF) antibody therapy saw remarkable progress in IBD therapy. Some patients, however, do not respond to anti-TNF treatment, or their response decreases over time. This phenomenon highlights the need to identify new molecular targets for therapy in IBD. The targets of new therapeutic molecules in IBD must aim to restore immune dysregulation by the inhibition of proinflammatory cytokines (TNF-α, interleukin [IL]-6, IL-13, IL-17, IL-18, and IL-21) and augmentation of the effect of anti-inflammatory cytokines (IL-10, IL-11, and transforming growth factor β) and to pursue new anti-inflammatory targets, such as regulatory T-cell therapy, Smad7 antisense, Janus-activated kinase inhibition, Toll-like receptor stimulation, leukocyte adhesion, and blockade of T-cell homing via integrins and mucosal addressin cellular adhesion molecule-1...
May 11, 2017: Gut and Liver
https://www.readbyqxmd.com/read/28486191/nlrp4-is-an-essential-negative-regulator-of-fructose-induced-cardiac-injury-in-vitro-and-in-vivo
#19
Yong-Gang Lian, Hai-Ying Zhao, Sheng-Ji Wang, Qin-Liang Xu, Xiang-Jun Xia
High fructose consumption leads to metabolic syndrome and enhances cardiovascular disease risk. However, our knowledge of the molecular mechanism underlying the cardiac disease caused by fructose feeding is still poor. Nod-like receptors (NLRs) are intracellular sensors, responding to a variety of intracellular danger signals to induce injuries. NLRP4 is a negative regulator of nuclear factor-κB (NF-κB) signaling pathway through interactions with kinase IκB kinase (IKK). Here, we illustrated that NLRP4 attenuates pro-inflammatory cytokines releasing, including Transforming growth factor (TGF-β1), Tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-18 (IL-18) and interleukin-6 (IL-6), in fructose-treated cardiac cells by means of RT-qPCR, and western blotting analysis...
May 6, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28484464/altered-natural-killer-cell-function-in-hiv-exposed-uninfected-infants
#20
Christiana Smith, Emilie Jalbert, Volia de Almeida, Jennifer Canniff, Laurel L Lenz, Marisa M Mussi-Pinhata, Rachel A Cohen, Qilu Yu, Fabiana R Amaral, Jorge Pinto, Jorge O Alarcon, George Siberry, Adriana Weinberg
OBJECTIVES: HIV-exposed uninfected (HEU) infants have higher rates of severe and fatal infections compared with HIV-unexposed (HUU) infants, likely due to immune perturbations. We hypothesized that alterations in natural killer (NK) cell activity might occur in HEU infants and predispose them to severe infections. DESIGN: Case-control study using cryopreserved peripheral blood mononuclear cells (PBMCs) at birth and 6 months from HEU infants enrolled from 2002 to 2009 and HUU infants enrolled from 2011 to 2013...
2017: Frontiers in Immunology
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