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NOD like receptor

Jinming Zhu, Miao He, Chunling Ma, Fengyun Peng, Yuli Su, Lei Huang
BACKGROUND In this study, we aimed to investigate the expression of NOD-like receptor protein 3 (NLRP3) and caspase-1 in fetal membrane and placental tissues of patients with premature rupture of membrane (PROM), and to explore their role in PROM. MATERIAL AND METHODS Ninety women participated in this study: a control group of 30 healthy pregnant women, 30 with PPROM, and 30 with TPROM. Immunohistochemistry streptavidin-peroxidase (SP) assay was used to detect the protein expression of NLRP3 and caspase-1 in the fetal membrane and placental tissues...
March 16, 2018: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
Allison E Irvin, Gaurang Jhala, Yuxing Zhao, Timothy S Blackwell, Balasubramanian Krishnamurthy, Helen E Thomas, Thomas W H Kay
Type 1 diabetes is an autoimmune disease characterised by selective destruction of pancreatic beta cells by the immune system. The transcription factor nuclear factor-kappa B (NF-κB) regulates innate and adaptive immune responses. Using gene targeting and in vitro analysis of pancreatic islets and immune cells, NF-κB activation has been implicated in type 1 diabetes development. Here we use a non-obese diabetic (NOD) mouse model that expresses a luciferase reporter of transcriptionally active NF-κB to determine its activation in vivo during development of diabetes...
March 9, 2018: Scientific Reports
Ariadne Androulidaki, Laurens Wachsmuth, Apostolos Polykratis, Manolis Pasparakis
Type 1 diabetes (T1D) is caused by the autoimmune destruction of the insulin-producing pancreatic beta cells. While the role of adaptive immunity has been extensively studied, the role of innate immune responses and particularly of Toll- like Receptor (TLR) signaling in T1D remains poorly understood. Here we show that myeloid cell-specific MyD88 deficiency considerably protected mice from the development of streptozotocin (STZ)-induced diabetes. The protective effect of MyD88 deficiency correlated with increased expression of the immunoregulatory enzyme indoleamine 2,3-dioxygenase (IDO) in pancreatic lymph nodes from STZ-treated mice and in bone marrow-derived dendritic cells (BMDC) stimulated with apoptotic cells...
2018: PloS One
Althea Campuzano, Floyd L Wormley
Cryptococcus species, the etiological agents of cryptococcosis, are encapsulated fungal yeasts that predominantly cause disease in immunocompromised individuals, and are responsible for 15% of AIDS-related deaths worldwide. Exposure follows the inhalation of the yeast into the lung alveoli, making it incumbent upon the pattern recognition receptors (PRRs) of pulmonary phagocytes to recognize highly conserved pathogen-associated molecular patterns (PAMPS) of fungi. The main challenges impeding the ability of pulmonary phagocytes to effectively recognize Cryptococcus include the presence of the yeast's large polysaccharide capsule, as well as other cryptococcal virulence factors that mask fungal PAMPs and help Cryptococcus evade detection and subsequent activation of the immune system...
March 7, 2018: Journal of Fungi (Basel, Switzerland)
Hua Ye, Shijun Xiao, Xiaoqing Wang, Zhiyong Wang, Zhengshi Zhang, Chengke Zhu, Bingjie Hu, Changhuan Lv, Shuming Zheng, Hui Luo
Schizothorax prenanti (S. prenanti) is an indigenous fish species and is popularly cultured in southwestern China. In recent years, intensive farming of S. prenanti and water quality deterioration has increased the susceptibility of this fish to various pathogens, including Aeromonas hydrophila (A. hydrophila), which has caused severe damage to S. prenanti production. However, the understanding of molecular immune response of S. prenanti to A. hydrophila infection is still lacking. In order to better comprehend the S...
March 8, 2018: Marine Biotechnology
Arpeeta Sharma, Mitchel Tate, Geetha Mathew, James E Vince, Rebecca H Ritchie, Judy B de Haan
It is now increasingly appreciated that inflammation is not limited to the control of pathogens by the host, but rather that sterile inflammation which occurs in the absence of viral or bacterial pathogens, accompanies numerous disease states, none more so than the complications that arise as a result of hyperglycaemia. Individuals with type 1 or type 2 diabetes mellitus (T1D, T2D) are at increased risk of developing cardiac and vascular complications. Glucose and blood pressure lowering therapies have not stopped the advance of these morbidities that often lead to fatal heart attacks and/or stroke...
2018: Frontiers in Physiology
Lotte Kors, Elena Rampanelli, Geurt Stokman, Loes Butter, Ntsiki M Held, Nike Claessen, Per W B Larsen, Joanne Verheij, Coert J Zuurbier, Gerhard Liebisch, Gerd Schmitz, Stephen E Girardin, Sandrine Florquin, Riekelt H Houtkooper, Jaklien C Leemans
NOD-like receptor (NLR)X1 (NLRX1) is an ubiquitously expressed inflammasome-independent NLR that is uniquely localized in mitochondria with as yet unknown effects on metabolic diseases. Here, we report that NLRX1 is essential in regulating cellular metabolism in non-immune parenchymal hepatocytes by decreasing mitochondrial fatty acid-dependent oxidative phosphorylation (OXPHOS) and promoting glycolysis. NLRX1 loss in mice has a profound impact on the prevention of diet-induced metabolic syndrome parameters, non-alcoholic fatty liver disease (NAFLD) progression, and renal dysfunction...
March 4, 2018: Biochimica et Biophysica Acta
Hiroyuki Nakayama, Kinya Otsu
Mitochondria play a central role in multiple cellular functions, including energy production, calcium homeostasis, and cell death. Currently, growing evidence indicates the vital roles of mitochondria in triggering and maintaining inflammation. Chronic inflammation without microbial infection - termed sterile inflammation - is strongly involved in the development of heart failure. Sterile inflammation is triggered by the activation of pattern recognition receptors (PRRs) that sense endogenous ligands called damage-associated molecular patterns (DAMPs)...
March 6, 2018: Biochemical Journal
Huiling Zhu, Haibo Wang, Shuhui Wang, Zhixiao Tu, Lin Zhang, Xiuying Wang, Yongqing Hou, Chunwei Wang, Jie Chen, Yulan Liu
SCOPE: Flaxseed oil is a rich source of α-linolenic acid (ALA), which is the precursor of the long-chain n-3 polyunsaturated fatty acids (PUFAs) including docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). This study investigated the protective effect of flaxseed oil against intestinal injury induced by lipopolysaccharide (LPS). MATERIALS AND RESULTS: Twenty-four weaned pigs were used in a 2 × 2 factorial experiment with dietary treatment (5% corn oil vs...
March 6, 2018: Molecular Nutrition & Food Research
Xiao Xu, Shaokui Chen, Haibo Wang, Zhixiao Tu, Shuhui Wang, Xiuying Wang, Huiling Zhu, Chunwei Wang, Jiadong Zhu, Yulan Liu
This study was conducted to evaluate whether medium-chain TAG (MCT) could alleviate Escherichia coli lipopolysaccharide (LPS)-induced intestinal injury by regulating intestinal epithelial inflammatory response, as well as necroptosis. A total of twenty-four weanling piglets were randomly allotted to one of four treatments in a 2×2 factorial arrangement including diet type (5 % maize oil v. 4 % MCT+1 % maize oil) and immune stress (saline v. E. coli LPS). The piglets were fed diets containing maize oil or MCT for 21 d...
March 6, 2018: British Journal of Nutrition
Min-Seok Kim, Jin-Young Han, Sung-Hwan Kim, Doin Jeon, Hyeon-Young Kim, Seung Woong Lee, Mun-Chual Rho, Kyuhong Lee
Oleanolic acid acetate (OAA), triterpenoid compound isolated from Vigna angularis (azuki bean), has been revealed anti-inflammatory in several studies. We investigated the effects of OAA against polyhexamethylene guanidine phosphate (PHMG-P)-induced pulmonary inflammation and fibrosis in mice. OAA treatment effectively alleviated PHMG-P-induced lung injury, including the number of total and differential cell in BAL fluid, histopathological lesions and hydroxyproline content in a dose dependent manner. Moreover, OAA treatment significantly decreased the elevations of IL-1β, IL-6, TNF-α, TGF-β1, and fibronectin, and the activation of the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome in the lungs of PHMG-P-treated mice...
March 2, 2018: Respiratory Physiology & Neurobiology
Gagandeep Kaur, Prathyusha Bagam, Rakeysha Pinkston, Dhirendra P Singh, Sanjay Batra
Chronic obstructive pulmonary disease (COPD) is a progressive, life-threatening disease that causes irreversible lung damage. Cigarette smoking is the chief etiologic factor for the commencement of this condition. Despite constant efforts to develop therapeutic interventions and to ascertain the molecular mechanism leading to the pathophysiology of this disease, much remains unknown. However, pattern recognition receptor (PRRs), i.e., Toll-like-receptors (TLRs) and NOD-like receptors (NLRs) are believed to play important roles in this disease and could serve as effective therapeutic targets...
February 28, 2018: Toxicology
R K Subbarao Malireddi, Prajwal Gurung, Jayadev Mavuluri, Tejasvi Krishna Dasari, Jeffery M Klco, Hongbo Chi, Thirumala-Devi Kanneganti
The NOD-like receptor (NLR)-P3 inflammasome is a global sensor of infection and stress. Elevated NLRP3 activation levels are associated with human diseases, but the mechanisms controlling NLRP3 inflammasome activation are largely unknown. Here, we show that TGF-β activated kinase-1 (TAK1) is a central regulator of NLRP3 inflammasome activation and spontaneous cell death. Absence of TAK1 in macrophages induced spontaneous activation of the NLRP3 inflammasome without requiring toll-like receptor (TLR) priming and subsequent activating signals, suggesting a distinctive role for TAK1 in maintaining NLRP3 inflammasome homeostasis...
March 2, 2018: Journal of Experimental Medicine
Jing Xiao, Xiaoli Zhang, Chensheng Fu, Qingmei Yang, Ying Xie, Zhenxing Zhang, Zhibin Ye
Hyperuricemia contributes to renal inflammation. We aimed to investigate the role of Na+ -K+ -ATPase (NKA) in hyperuricemia-induced renal tubular injury. Human primary proximal tubular epithelial cells (PTECs) were incubated with uric acid (UA) at increasing doses or for increasing lengths of time. PTECs were then stimulated by pre-incubation with an NKA α1 expression vector or small interfering RNA before UA (100 μg ml-1 , 48 h) stimulation. Hyperuricemic rats were induced by gastric oxonic acid and treated with febuxostat (Feb)...
March 2, 2018: Experimental & Molecular Medicine
Sanaz Nasoohi, Saifudeen Ismael, Tauheed Ishrat
Neurological diseases, including acute attacks (e.g., ischemic stroke) and chronic neurodegenerative diseases (e.g., Alzheimer's disease), have always been one of the leading cause of morbidity and mortality worldwide. These debilitating diseases represent an enormous disease burden, not only in terms of health suffering but also in economic costs. Although the clinical presentations differ for these diseases, a growing body of evidence suggests that oxidative stress and inflammatory responses in brain tissue significantly contribute to their pathology...
February 27, 2018: Molecular Neurobiology
Mary-Anne Hartley, Remzi O Eren, Matteo Rossi, Florence Prevel, Patrik Castiglioni, Nathalie Isorce, Chantal Desponds, Lon-Fye Lye, Stephen M Beverley, Stefan K Drexler, Nicolas Fasel
The various symptomatic outcomes of cutaneous leishmaniasis relates to the type and potency of its underlying inflammatory responses. Presence of the cytoplasmic Leishmania RNA virus-1 (LRV1) within Leishmania guyanensis , worsens lesional inflammation and parasite burden, as the viral dsRNA genome acts as a potent innate immunogen stimulating Toll-Like-Receptor-3 (TLR3). Here we investigated other innate pattern recognition receptors capable of reacting to dsRNA and potentially contributing to LRV1-mediated inflammatory pathology...
January 14, 2018: Microbial Cell
Ying Meng, Miao-Xia Pan, Bo-Jun Zheng, Yan Chen, Wei Li, Qian-Jie Yang, Ze-Mao Zheng, Na-Na Sun, Yue Zhang, Xu Li
<b><i>Aims:</i></b> The NLRP3 (NOD-like receptor family pyrin domain containing 3) inflammasome, which is activated by reactive oxygen species (ROS) and respressed by autophagy, has been identified as a novel agent of pulmonary fibrosis. Angiotensin II (AngII), the bioactive pro-oxidant in the renin-angiotensin system (RAS), aggravates lung fibrosis. However, the effect of AngII on NLRP3 inflammasome and autophagy in lung fibrosis remains unknown. <i><b>Objective:</b></i> To investigate a potential link between AngII, redox balance, autophagy and the NLRP3 inflammasome, which determines extracellular matrix accumulation in lung fibrosis...
February 27, 2018: Antioxidants & Redox Signaling
Alessandra Bandera, Michela Masetti, Massimiliano Fabbiani, Mara Biasin, Antonio Muscatello, Nicola Squillace, Mario Clerici, Andrea Gori, Daria Trabattoni
Background: Inflammasome-mediated activation of caspase-1 regulates inflammatory responses and pyroptosis. We analyzed possible associations between inflammasome-related genes and immune reconstitution in HIV-infected antiretroviral therapy (ART)-treated patients. Methods: Cross-sectional, case-control study. HIV-infected patients on ART for ≥24 months with HIV-RNA<50 cp/mL for ≥12 months were enrolled and defined as immunological responders (IR) or non-responders (INR) if CD4 count was ≥500 or ≤350 cells/μL, respectively...
2018: Frontiers in Immunology
Anna Negroni, Maria Pierdomenico, Salvatore Cucchiara, Laura Stronati
The nucleotide-binding oligomerization domain (NOD) protein, NOD2, belonging to the intracellular NOD-like receptor family, detects conserved motifs in bacterial peptidoglycan and promotes their clearance through activation of a proinflammatory transcriptional program and other innate immune pathways, including autophagy and endoplasmic reticulum stress. An inactive form due to mutations or a constitutive high expression of NOD2 is associated with several inflammatory diseases, suggesting that balanced NOD2 signaling is critical for the maintenance of immune homeostasis...
2018: Journal of Inflammation Research
Islam N Mohamed, Nahla Reda Sarhan, Mohamed Ahmed Eladl, Azza B El-Remessy, Mohamed El-Sherbiny
Endemic prevalence of obesity is associated with alarming increases in non-alcoholic steatohepatitis (NASH) with limited available therapeutics. Toll-like receptor2 (TLR2) and Nod-like receptor protein 3 (NLRP3) Inflammasome are implicated in hepatic steatosis, inflammation and fibrosis; the histological landmark stages of NASH. TXNIP, a member of α-arrestin family activates NLRP3 in response to various danger stimuli. The aim of current work was to investigate the effect of TXNIP genetic deletion on histological manifestations of high fat diet-induced steatohepatitis and activation of TLR2-NLRP3-inflammasome axis...
February 23, 2018: Acta Histochemica
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