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[PMID]: 29524428
[Au] Autor:Ploscariu NT; de Jong NWM; van Kessel KPM; van Strijp JAG; Geisbrecht BV
[Ad] Address:Department of Biochemistry & Molecular Biophysics, Kansas State University, 141 Chalmers Hall, 1711 Claflin Road, Manhattan, KS, 66506, USA.
[Ti] Title:Identification and structural characterization of a novel myeloperoxidase inhibitor from Staphylococcus delphini.
[So] Source:Arch Biochem Biophys;, 2018 Mar 07.
[Is] ISSN:1096-0384
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Staphylococcus aureus and related species are highly adapted to their hosts and have evolved numerous strategies to evade the immune system. S. aureus shows resistance to killing following uptake into the phagosome, which suggests that the bacterium evades intracellular killing mechanisms used by neutrophils. We recently discovered an S. aureus protein (SPIN for Staphylococcal Peroxidase INhibitor) that binds to and inhibits myeloperoxidase (MPO), a major player in the oxidative defense of neutrophils. To allow for comparative studies between multiple SPIN sequences, we identified a panel of homologs from species closely related to S. aureus. Characterization of these proteins revealed that SPIN molecules from S. agnetis, S. delphini, S. schleiferi, and S. intermedius all bind human MPO with nanomolar affinities, and that those from S. delphini, S. schleiferi, and S. intermedius inhibit human MPO in a dose-dependent manner. A 2.4 Šresolution co-crystal structure of SPIN-delphini bound to recombinant human MPO allowed us to identify conserved structural features of SPIN proteins, and to propose sequence-dependent physical explanations for why SPIN-aureus binds human MPO with higher affinity than SPIN-delphini. Together, these studies expand our understanding of MPO binding and inhibition by a recently identified component of the staphylococcal innate immune evasion arsenal.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 112331 MEDLINE  
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[PMID]: 29524409
[Au] Autor:Norris PC; Serhan CN
[Ad] Address:Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, 60 Fenwood Road, BTM 3016, Boston, MA, 02115, USA.
[Ti] Title:Metabololipidomic profiling of functional immunoresolvent clusters and eicosanoids in mammalian tissues.
[So] Source:Biochem Biophys Res Commun;, 2018 Mar 07.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Metabolomics enables a systems approach to interrogate the bioactive mediators, their pathways and further metabolites involved in the physiology and pathophysiology of human and animal tissues. New metabololipidomic approaches with mass spectrometry presented in this brief review can now be utilized for the identification and profiling of lipid mediator networks that control inflammation-resolution in human blood and healthy and diseased solid tissues. Coagulation of blood is a protective response that prevents excessive bleeding on injury of blood vessels. Here, we review novel approaches to understand the relationship(s) between coagulation and resolution of inflammation and infection. To determine whether coagulation is involved in host-protective actions by lipid mediators, we used a metabololipidomic-based profiling approach with human whole blood (WB) during coagulation. We identified recently temporal clusters of endogenously produced pro-thrombotic and proinflammatory lipid mediators (eicosanoids), as well as specialized proresolving mediators (SPMs) in this vital process. In addition to the classic eicosanoids (prostaglandins, thromboxanes and leukotrienes), a specific SPM cluster was identified that consists of resolvin E1 (RvE1), RvD1, RvD5, lipoxin B , and maresin 1, each of which present at bioactive concentrations (0.1-1 nM). The removal of adenosine from coagulating blood samples significantly enhances SPM amounts and unleashes the biosynthesis of RvD3, RvD4, and RvD6 evident following rapid snap freezing with centrifugation before extraction and LC-MS-MS. The classic cyclooxygenase inhibitors, celecoxib and indomethacin, that block thromboxanes and prostanoids do not block production of the clot-driven SPM cluster. Unbiased mass cytometry analysis demonstrated that the SPM cluster produced in human blood targets leukocytes at the single-cell level, directly activating extracellular signaling in human neutrophils and monocytes. Human whole blood treated with the components of this SPM cluster enhanced both phagocytosis and killing of Escherichia coli by leukocytes. Thus, we identified a pro-resolving lipid mediator circuit and specific SPM cluster that promotes host defense. This new lipid mediator (LM)-SPM metabololipidomic approach now provides accessible metabolomic profiles in healthy and diseased human tissues, including cancer, for precision and personalized medicine.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 112331 MEDLINE  
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[PMID]: 29496577
[Au] Autor:Zhao YL; Yang ZF; Shang JH; Huang WY; Wang B; Wei X; Khan A; Yuan ZW; Liu YP; Wang YF; Wang XH; Luo XD
[Ad] Address:State Key Laboratory of Phytochemistry and Plant Resources in West China, Kunming Institute of Botany, Chinese Academy of Sciences, Kunming 650201, China.
[Ti] Title:Effects of indole alkaloids from leaf of Alstonia scholaris on post-infectious cough in mice.
[So] Source:J Ethnopharmacol;218:69-75, 2018 Feb 26.
[Is] ISSN:1872-7573
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:ETHNOPHARMACOLOGICAL RELEVANCE: Leaf of Alstonia scholaris (L.) R. Br. (Apocynaceae), a wide used ethic-medicine in many Asia and Africa counties, has also been recorded as the common traditional Chinese medicine for treatment of illnesses in respiratory system by Dai people. AIM OF THE STUDY: To provide experimental data of clinical adaption of total indole alkaloids (TA) from leaf of A. scholaris for treating post-infectious cough in phase II clinical trial. MATERIALS AND METHODS: To model post-infectious cough, all animals except control group were instilled intra-tracheal with lipopolysaccharide (LPS) (80 µg/50 µL/mouse), followed by subsequent exposure to cigarette smoke (CS) for 30 min per day for a total of 30 days. Mice were orally given TA at dose of 10, 25, 50 mg/kg, and four main alkaloids (Sch: scholaricine, Epi: 19-epischolaricine, Val: vallesamine, Pic: picrinine) once daily. Cellular infiltration was assessed in the broncho-alveolar lavage fluid (BALF). Expression of interleukin-6 (IL-6) and C-reactive protein (CRP) in the serum was determined, the superoxide dismutase (SOD) activity as well as malondialdehyde (MDA) content in the serum and homogenate were examined. Finally, histopathological examination in the lungs was assessed by H. E. staining. RESULTS: After administration of TA and four major alkaloids respectively, the symptoms of cough in mice were obviously attenuated. Total white blood cells (WBC) and neutrophils (NEU) amounts in BALF were reduced obviously and the pathological damage of lung was also attenuated. There was also significant reduction in IL-6, CRP, MDA and a marked improvement in SOD. CONCLUSIONS: The efficacy of indole alkaloids against post-infectious cough (PIC) was shown in the down-regulation of inflammatory cells, cytokines, and the balance of antioxidants. What's more, the pharmacological effects of TA were better than single indole alkaloid, which might be related to the synergic effect of four major alkaloids.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 112331 MEDLINE  
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[PMID]: 29486352
[Au] Autor:Xu C; Li E; Suo Y; Su Y; Lu M; Zhao Q; Qin JG; Chen L
[Ad] Address:Department of Aquaculture, College of Marine Sciences, Hainan University, Haikou, Hainan 570228, China; School of Life Sciences, East China Normal University, Shanghai 200241, China.
[Ti] Title:Histological and transcriptomic responses of two immune organs, the spleen and head kidney, in Nile tilapia (Oreochromis niloticus) to long-term hypersaline stress.
[So] Source:Fish Shellfish Immunol;76:48-57, 2018 Feb 24.
[Is] ISSN:1095-9947
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Hyperosmotic stress can adversely affect fish immunity, but little is known about the histological and transcriptomic responses of immune organs in fish in a hyperosmotic environment. This study evaluated the effects of long-term hypersaline conditions (16‰) on the growth, histology and transcriptomics of the two main immune organs, the spleen and head kidney, in Nile tilapia Oreochromis niloticus relative to those reared in freshwater for eight weeks. No differences in weight gain and specific growth rate were found between fish reared under these two salinities. Hyperosmotic stress induced a congestive or enlarged spleen. Platelet- and coagulation-related gene expression was significantly decreased in tilapia at 16‰. The red cell distribution width and value of the mean corpuscular hemoglobin were significantly greater in fish at 16‰ salinity than in control fish in freshwater. A large volume of melano-macrophages in the spleen and pigment deposition in both the spleen and head kidney were observed in the histological sections in fish at 16‰ salinity. Transmission electron microscopic results showed abnormal macrophages with deposition granules in the spleen and head kidney and more neutrophils in the head kidney of fish at 16‰ than in control fish. In total, 772 and 502 genes were annotated for significantly different expression in the spleen and head kidney, respectively, and corresponded to five and one significantly changed immune system pathways, respectively. The complement pathway in the spleen was significantly down-regulated at 16‰. This study indicates that long-term exposure of Nile tilapia to a hyperosmotic environment can induce splenomegaly, reduce coagulation function, enhance phagocytic activity and down-regulate the complement pathway in the spleen. The spleen is a more sensitive organ for immune responses to chronic ambient salinity stress than the head kidney in Nile tilapia.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 112331 MEDLINE  
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[PMID]: 29481961
[Au] Autor:Bagheri N; Razavi A; Pourgheysari B; Azadegan-Dehkordi F; Rahimian G; Pirayesh A; Shafigh M; Rafieian-Kopaei M; Fereidani R; Tahmasbi K; Shirzad H
[Ad] Address:Cellular and Molecular Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran.
[Ti] Title:Up-regulated Th17 cell function is associated with increased peptic ulcer disease in Helicobacter pylori-infection.
[So] Source:Infect Genet Evol;60:117-125, 2018 Feb 23.
[Is] ISSN:1567-7257
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: During Helicobacter pylori (H. pylori) infection CD4 T cells in the gastric lamina propria are hyporesponsive and polarized by Th1/Th17 cell responses controlled by Treg cells. The objective of this study was to determine the number of Th17 cells in gastric mucosa of patients with gastritis and peptic ulcer and determined the relationship between main virulence factor of H. pylori and Th17 cells. METHODS AND MATERIALS: A total of 89 H. pylori-infected gastritis patients, 63 H. pylori-infected peptic ulcer patients and 48 H. pylori-negative non-ulcer dysplasia patients were enrolled in this study. The number of Th17 was determined by immunohistochemistry. IL-8 and IL-17A expressions were determined by real-time polymerase chain reaction (qPCR). Also, the grade of chronic and active inflammation was investigated for involvement according to the density of neutrophils and mononuclear in gastric mucosal crypts, from one to all crypts. RESULTS: The number of Th17 cells and the expression of IL-8 and IL-17A in infected patients were significantly higher than uninfected subjects. The number of Th17 cells and the expression of IL-8 and IL-17A in infected patients with peptic ulcer were significantly higher than patients with gastritis. Additionally, the numbers of Th17 cells as well as the expression of IL-8 and IL-17A were positively correlated with the degree of H. pylori density in infected patients with peptic ulcer, while this correlation was negative in infected patients with gastritis. The numbers of Th17 cells as well as the expression of IL-8 and IL-17A were positively correlated with the degree of chronic inflammation. CONCLUSION: The predominant Th17 cell responses may play a role in the pathogenesis of peptic ulcers disease in infected patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 112331 MEDLINE  
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[PMID]: 29477577
[Au] Autor:Sundqvist M; Christenson K; Holdfeldt A; Gabl M; Mårtensson J; Björkman L; Dieckmann R; Dahlgren C; Forsman H
[Ad] Address:Department of Rheumatology and Inflammation Research, Sahlgrenska, Academy, University of Gothenburg, Gothenburg, Sweden.
[Ti] Title:Similarities and differences between the responses induced in human phagocytes through activation of the medium chain fatty acid receptor GPR84 and the short chain fatty acid receptor FFA2R.
[So] Source:Biochim Biophys Acta;1865(5):695-708, 2018 Feb 22.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:GPR84 is a recently de-orphanized member of the G-protein coupled receptor (GPCR) family recognizing medium chain fatty acids, and has been suggested to play important roles in inflammation. Due to the lack of potent and selective GPR84 ligands, the basic knowledge related to GPR84 functions is very limited. In this study, we have characterized the GPR84 activation profile and regulation mechanism in human phagocytes, using two recently developed small molecules that specifically target GPR84 agonistically (ZQ16) and antagonistically (GLPG1205), respectively. Compared to our earlier characterization of the short chain fatty acid receptor FFA2R which is functionally expressed in neutrophils but not in monocytes, GPR84 is expressed in both cell types and in monocyte-derived macrophages. In neutrophils, the GPR84 agonist had an activation profile very similar to that of FFA2R. The GPR84-mediated superoxide release was low in naïve cells, but the response could be significantly primed by TNFα and by the actin cytoskeleton disrupting agent Latrunculin A. Similar to that of FFA2R, a desensitization mechanism bypassing the actin cytoskeleton was utilized by GPR84. All ZQ16-mediated cellular responses were sensitive to GLPG1205, confirming the GPR84-dependency. Finally, our data of in vivo transmigrated tissue neutrophils indicate that both GPR84 and FFA2R are involved in neutrophil recruitment processes in vivo. In summary, we show functional similarities but also some important differences between GPR84 and FFA2R in human phagocytes, thus providing some mechanistic insights into GPR84 regulation in blood neutrophils and cells recruited to an aseptic inflammatory site in vivo.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 112331 MEDLINE  
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[PMID]: 29476818
[Au] Autor:Harikrishnan R; Jawahar S; Thamizharasan S; Paray BA; Al-Sadoon MK; Balasundaram C
[Ad] Address:Department of Zoology, Pachaiyappa's College for Men, Kanchipuram, 631 501, Tamil Nadu, India. Electronic address: rhari123@yahoo.com.
[Ti] Title:Immune defense of emodin enriched diet in Clarias batrachus against Aeromonas hydrophila.
[So] Source:Fish Shellfish Immunol;76:13-20, 2018 Feb 21.
[Is] ISSN:1095-9947
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:This study investigates the effect of emodin enriched diet on growth, hematology, and immune response in walking catfish, Clarias batrachus against Aeromonas hydrophila. The basal (control) diet supplemented with emodin at 0.0, 0.1, 0.2, or 0.4 g kg was fed to the experimental groups for a period of four weeks. Feeding infected fish with 0.2 g kg and 0.4 g kg emodin enriched diets resulted in an overall weight gain, enhanced PER and FCR when compared to other diets. The survival rates were 98.3% and 96.7% in 0.1 g kg and 0.4 g kg emodin diet fed groups. Feeding with 0.2 g kg diet the RBC level significantly elevated on week 1 and with 0.4 g kg diet on weeks 2 and 4. The WBC, the percentage of globulin and neutrophils increased significantly with 0.2 g kg diet only on week 4; however with 0.4 g kg diet the increase was observed from week 1-4. The phagocytic activity increased significantly on being fed with 0.4 g kg diet on week 2 while with 0.2 g kg and 0.4 g kg diets the increase manifested only on week 4; the respiratory burst activity also significantly increased on week 4 whereas increased the complement activity on weeks 2 and 4. The superoxide dismutase (SOD) activity was high on being fed with 0.4 g kg diet on week 1; with 0.2 g kg or 0.4 g kg diets the increase was observed on weeks 2 and 4. The serum IgM level significantly increased when fed with 0.4 g kg diet whereas the lysozyme activity was enhanced with 0.2 g kg and 0.4 g kg emodin diets on weeks 2 and 4. The percentage cumulative mortality was 10% with 0.1 g kg or 0.2 g kg diets while with 0.2 g kg diet it was 15%. The results demonstrate that as a feed additive emodin acts as an immunostimulant enhancing the specific and nonspecific immune defense affording increased disease protection, enhances better growth and boosts hematology parameters in C. batrachus against A. hydrophila infection.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  8 / 112331 MEDLINE  
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[PMID]: 29476479
[Au] Autor:Evans MA; Kim HA; Ling YH; Uong S; Vinh A; De Silva TM; Arumugam TV; Clarkson AN; Zosky GR; Drummond GR; Broughton BRS; Sobey CG
[Ad] Address:Vascular Biology Immunopharmacology Group, Department of Physiology, Anatomy and Microbiology, La Trobe University, Bundoora, VIC, 3083, Australia.
[Ti] Title:Vitamin D Supplementation Reduces Subsequent Brain Injury and Inflammation Associated with Ischemic Stroke.
[So] Source:Neuromolecular Med;20(1):147-159, 2018 Mar.
[Is] ISSN:1559-1174
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Acute inflammation can exacerbate brain injury after ischemic stroke. Beyond its well-characterized role in calcium metabolism, it is becoming increasingly appreciated that the active form of vitamin D, 1,25-dihydroxyvitamin D (1,25-VitD ), has potent immunomodulatory properties. Here, we aimed to determine whether 1,25-VitD supplementation could reduce subsequent brain injury and associated inflammation after ischemic stroke. Male C57Bl6 mice were randomly assigned to be administered either 1,25-VitD (100 ng/kg/day) or vehicle i.p. for 5 day prior to stroke. Stroke was induced via middle cerebral artery occlusion for 1 h followed by 23 h reperfusion. At 24 h post-stroke, we assessed infarct volume, functional deficit, expression of inflammatory mediators and numbers of infiltrating immune cells. Supplementation with 1,25-VitD reduced infarct volume by 50% compared to vehicle. Expression of pro-inflammatory mediators IL-6, IL-1ß, IL-23a, TGF-ß and NADPH oxidase-2 was reduced in brains of mice that received 1,25-VitD versus vehicle. Brain expression of the T regulatory cell marker, Foxp3, was higher in mice supplemented with 1,25-VitD versus vehicle, while expression of the transcription factor, ROR-γ, was decreased, suggestive of a reduced Th17/γδ T cell response. Immunohistochemistry indicated that similar numbers of neutrophils and T cells were present in the ischemic hemispheres of 1,25-VitD - and vehicle-supplemented mice. At this early time point, there were also no differences in the impairment of motor function. These data indicate that prior administration of exogenous vitamin D, even to vitamin D-replete mice, can attenuate infarct development and exert acute anti-inflammatory actions in the ischemic and reperfused brain.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1007/s12017-018-8484-z

  9 / 112331 MEDLINE  
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[PMID]: 29432911
[Au] Autor:Yang J; Tian H; Huang X
[Ad] Address:Emergency Department, Guizhou Provincial People's Hospital, Guiyang, Guizhou, 550002, China.
[Ti] Title:Tephrosin attenuates sepsis induced acute lung injury in rats by impeding expression of ICAM-1 and MIP-2.
[So] Source:Microb Pathog;117:93-99, 2018 Feb 09.
[Is] ISSN:1096-1208
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Acute lung injury (ALI), a devastating form of respiratory infections, is characterized by increased edema, release of cytokines, weakened arterial oxygenation and infiltration of neutrophils and lymphocytes. The objective of the research envisaged was to reveal protective effects of tephrosin (TP) in ALI. In the present investigation, sepsis was triggered in rats by cecal ligation and puncture (CLP) method, and TP was administered intraperitonially. Five groups - Group A (control), Group B (Sham group) Group C (infected and untreated), and Group D and E (infected and treated with 25 and 50 mg/kg TP respectively) - of ten rats each, were used for the investigation. Evaluation parameters included measurement of arterial oxygenation, lung water content, protein determination, cytokine determination, neutrophil and lymphocyte count in the bronchoalveolar lavage fluid (BALF). As indicated by histopathological examination, the lung injury score was maximum in group C, but indicated reduction in group D and E. Intracellular adhesion molecule (ICAM)-1 and macrophage inflammatory protein-2 (MIP-2) are known to be important mediators responsible for ALI. Reduction in the ICAM-1 and MIP-2 expression was found to reduce after treatment with TP. In comparison to group D, group E reflected higher magnitude of ICAM-1 and MIP-2 suppression due to administration of higher TP dose. Compared to Group A and B, Group E indicated slightly higher expression of ICAM-1 and MIP-2. The research envisaged thus supports that TP attenuates ICAM-1 and MIP-2 expression in sepsis induced ALI rat model.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  10 / 112331 MEDLINE  
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[PMID]: 29524208
[Au] Autor:Pan P; Oshima K; Huang YW; Agle KA; Drobyski WR; Chen X; Zhang J; Yearsley MM; Yu J; Wang LS
[Ad] Address:Division of Hematology and Oncology, Department of Medicine, Medical College of Wisconsin, Milwaukee, WI, USA.
[Ti] Title:Loss of FFAR2 promotes colon cancer by epigenetic dysregulation of inflammation suppressors.
[So] Source:Int J Cancer;, 2018 Mar 09.
[Is] ISSN:1097-0215
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Free fatty acid receptor 2 (FFAR2, also named GPR43), is activated by short-chain fatty acids (SCFAs), such as butyrate, that are produced when gut bacteria ferment dietary fiber. FFAR2 has been suggested to regulate colonic inflammation, which is a major risk factor for the development of colon cancer and is also linked to epigenetic dysregulation in colon carcinogenesis. The current study assessed whether FFAR2, acting as an epigenetic regulator, protects against colon carcinogenesis. To mimic the mild inflammation that promotes human colon cancer, we treated mice with dextran sodium sulfate (DSS) overnight, which avoids excessive inflammation but induces mild inflammation that promotes colon carcinogenesis in the Apc and the azoxymethane (AOM)-treated mice. Our results showed that FFAR2 deficiency promotes the development of colon adenoma in the Apc /DSS mice and the progression of adenoma to adenocarcinoma in the AOM/DSS mice. FFAR2's downstream cAMP-PKA-CREB pathway was enhanced, leading to overexpression of histone deacetylases (HDACs) in the FFAR2-deficient mice. ChIP-qPCR analysis revealed differential binding of H3K27me3 and H3K4me3 histone marks onto the promoter regions of inflammation suppressors (e.g., sfrp1, dkk3, socs1), resulting in decreased expression of these genes in the FFAR2-deficient mice. Also, more neutrophils infiltrated into tumors and colon lamina propria of the FFAR2-deficient mice. Depletion of neutrophils blocked the progression of colon tumors. In addition, FFAR2 is required for butyrate to suppress HDAC expression and hypermethylation of inflammation suppressors. Therefore, our results suggest that FFAR2 is an epigenetic tumor suppressor that acts at multiple stages of colon carcinogenesis. This article is protected by copyright. All rights reserved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1002/ijc.31366


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