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[PMID]: 29524707
[Au] Autor:Nishimura F; Park YS; Motoyama Y; Nakagawa I; Yamada S; Nakase H
[Ad] Address:Department of Neurosurgery, Nara Medical University, Nara, Japan. Electronic address: fnishi@naramed-u.ac.jp.
[Ti] Title:Pediatric case of xanthogranuloma in sellar region presenting visual disturbance successfully treated by endoscopic endonasal surgery.
[So] Source:World Neurosurg;, 2018 Mar 07.
[Is] ISSN:1878-8769
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Xanthomatous pituitary diseases rarely occur in childhood. We report a rare pediatric case of a xanthogranuloma that developed in the sellar region resulting in visual disturbance that was successfully treated by endoscopic endonasal surgery. CASE DESCRIPTIONS: A 13-year-old boy came to us with a headache and visual disturbance that had occurred 1 month prior. Clinical examination findings showed that he was alert with signs of bitemporal hemianopsia, an endocrinological examination showed partial hypopituitarism, and brain magnetic resonance imaging (MRI) revealed a cystic mass in the sellar turcica compressing the optic apparatus. Endoscopic endonasal surgery was performed to decompress the optic apparatus and the mass was removed. Histopathological analysis of the tumor demonstrated granulomatous tissue with cholesterol clefts, foamy macrophages, and multinucleated giant cells, with no epithelial component. The diagnosis was xanthogranuloma of the sellar region. The patient gradually recovered from visual disturbance and was free from any neurological symptom 6 months after surgery. CONCLUSIONS: Xanthogranuloma, although rare, should be considered as a differential diagnosis of a sellar/suprasellar lesion even in children.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 206628 MEDLINE  
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[PMID]: 29524540
[Au] Autor:Mishra OP; Popov AV; Pietrofesa RA; Nakamaru-Ogiso E; Andrake M; Christofidou-Solomidou M
[Ad] Address:Department of Medicine, Pulmonary, Allergy and Critical Care Division, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19111, United States.
[Ti] Title:Synthetic secoisolariciresinol diglucoside (LGM2605) inhibits myeloperoxidase activity in inflammatory cells.
[So] Source:Biochim Biophys Acta;, 2018 Mar 07.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: Myeloperoxidase (MPO) generates hypochlorous acid (HOCl) during inflammation and infection. We showed that secoisolariciresinol diglucoside (SDG) scavenges radiation-induced HOCl in physiological solutions. However, the action of SDG and its synthetic version, LGM2605, on MPO-catalyzed generation of HOCl is unknown. The present study evaluated the effect of LGM2605 on MPO. METHODS: MPO activity was determined fluorometrically using hypochlorite-specific 3'-(p-aminophenyl) fluorescein (APF). The effect of LGM2605 on (a) the peroxidase cycle of MPO was determined using Amplex Red while the effect on (b) the chlorination cycle was determined using a taurine chloramine assay. Using electron paramagnetic resonance (EPR) spectroscopy we determined the effect of LGM2605 on the EPR signals of MPO. Finally, computational docking of SDG was used to identify energetically favorable docking poses to enzyme's active site. RESULTS: LGM2605 inhibited human and murine MPO activity. MPO inhibition was observed in the absence and presence of Cl . EPR confirmed that LGM2605 suppressed the formation of Compound I, an oxoiron (IV) intermediate [Fe(IV)O] containing a porphyrin π-radical of MPO's catalytic cycle. Computational docking revealed that SDG can act as an inhibitor by binding to the enzyme's active site. CONCLUSIONS: We conclude that LGM2605 inhibits MPO activity by suppressing both the peroxidase and chlorination cycles. EPR analysis demonstrated that LGM2605 inhibits MPO by decreasing the formation of the highly oxidative Compound I. This study identifies a novel mechanism of LGM2605 action as an inhibitor of MPO and indicates that LGM2605 may be a promising attenuator of oxidant-dependent inflammatory tissue damage.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 206628 MEDLINE  
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[PMID]: 29524539
[Au] Autor:Lejal N; Truchet S; Bechor E; Bouguyon E; Khedkar V; Bertho N; Vidic J; Adenot P; Solier S; Pick E; Slama-Schwok A
[Ad] Address:Paris Saclay University, U892 INRA, Jouy en Josas, France.
[Ti] Title:Turning off NADPH oxidase-2 by impeding p67 activation in infected mouse macrophages reduced viral entry and inflammation.
[So] Source:Biochim Biophys Acta;, 2018 Mar 07.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: Targeting cells of the host immune system is a promising approach to fight against Influenza A virus (IAV) infection. Macrophage cells use the NADPH oxidase-2 (NOX2) enzymatic complex as a first line of defense against pathogens by generating superoxide ions O and releasing H O . Herein, we investigated whether targeting membrane -embedded NOX2 decreased IAV entry via raft domains and reduced inflammation in infected macrophages. METHODS: Confocal microscopy and western blots monitored levels of the viral nucleoprotein NP and p67 , NOX2 activator subunit, Elisa assays quantified TNF-α levels in LPS or IAV-activated mouse or porcine alveolar macrophages pretreated with a fluorescent NOX inhibitor, called nanoshutter NS1. RESULTS: IAV infection in macrophages promoted p67 translocation to the membrane, rafts clustering and activation of the NOX2 complex at early times. Disrupting rafts reduced intracellular viral NP. NS1 markedly reduced raft clustering and viral entry by binding to the C-terminal of NOX2 also characterized in vitro. NS1 decrease of TNF-α release depended on the cell type. CONCLUSION: NOX2 participated in IAV entry and raft-mediated endocytosis. NOX2 inhibition by NS1 reduced viral entry. NS1 competition with p67 for NOX2 binding shown by in silico models and cell-free assays was in agreement with NS1 inhibiting p67 translocation to membrane-embedded NOX2 in mouse and porcine macrophages. GENERAL SIGNIFICANCE: We introduce NS1 as a compound targeting NOX2, a critical enzyme controlling viral levels and inflammation in macrophages and discuss the therapeutic relevance of targeting the C-terminal of NADPH oxidases by probes like NS1 in viral infections.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 206628 MEDLINE  
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[PMID]: 29524502
[Au] Autor:Nakagawa M; Uno S; Iriyama N; Matsunawa M; Makishima M; Takeuchi J; Tsuboi I; Hatta Y; Takei M
[Ad] Address:Division of Hematology and Rheumatology, Department of Medicine, Nihon University School of Medicine, 30-1 Oyaguchi-kamicho, Itabashi-ku, Tokyo 173-8610, Japan.
[Ti] Title:Combined treatment with benzo[a]pyrene and 1α,25-dihydroxyvitamin D induces expression of plasminogen activator inhibitor 1 in monocyte/macrophage-derived cells.
[So] Source:Toxicol Appl Pharmacol;, 2018 Mar 07.
[Is] ISSN:1096-0333
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Benzo[a]pyrene (BaP) is an environmental pollutant found in cigarette smoke and is implicated as a causative agent of tobacco-related diseases, such as arteriosclerosis. In contrast, vitamin D signaling, which is principally mediated by conversion of vitamin D to the active form, 1α,25-dihydroxyvitamin D [1,25(OH) D ], decreases cardiovascular disease risk. However, combined treatment with BaP and 1,25(OH) D enhances BaP toxicity, including BaP-DNA adduct formation. We further investigated the cross-talk between BaP and 1,25(OH) D signaling pathways, and found that combined treatment with these compounds induces mRNA and protein expression of plasminogen activator inhibitor 1 (PAI-1) in monocyte/macrophage-derived THP-1 and U937 cells. Protein synthesis inhibitor treatment did not inhibit induction of the PAI-1 gene (SERPINE1) in these cells. BaP plus 1,25(OH) D induced differentiation markers, inhibited cellular proliferation, and induced apoptosis and oxidative stress in these cells. Reactive oxygen species scavenger treatment suppressed apoptosis but not SERPINE1 induction in cells treated with BaP plus 1,25(OH) D . Thus, combined treatment with BaP and 1,25(OH) D induced SERPINE1 mRNA expression in these cells through a mechanism that does not require de novo protein synthesis or reactive oxygen species production. These findings suggest that induction of the proinflammatory factor PAI-1 plays a role in BaP toxicity. Interestingly, PAI-1 knockdown decreased expression of the cell surface antigen CD14, a monocytic differentiation marker, in THP-1 cells treated with BaP plus 1,25(OH) D . PAI-1 induction may also be related to a function of monocytes/macrophages in response to xenobiotic and vitamin D signaling.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 206628 MEDLINE  
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[PMID]: 29524441
[Au] Autor:Bowness R; Chaplain MAJ; Powathil GG; Gillespie SH
[Ad] Address:School of Medicine, University of St Andrews, North Haugh, St Andrews, KY16 9TF, UK. Electronic address: rec9@st-andrews.ac.uk.
[Ti] Title:Modelling the effects of bacterial cell state and spatial location on tuberculosis treatment: Insights from a hybrid multiscale cellular automaton model.
[So] Source:J Theor Biol;, 2018 Mar 07.
[Is] ISSN:1095-8541
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:If improvements are to be made in tuberculosis (TB) treatment, an increased understanding of disease in the lung is needed. Studies have shown that bacteria in a less metabolically active state, associated with the presence of lipid bodies, are less susceptible to antibiotics, and recent results have highlighted the disparity in concentration of different compounds into lesions. Treatment success therefore depends critically on the responses of the individual bacteria that constitute the infection. We propose a hybrid, individual-based approach that analyses spatio-temporal dynamics at the cellular level, linking the behaviour of individual bacteria and host cells with the macroscopic behaviour of the microenvironment. The individual elements (bacteria, macrophages and T cells) are modelled using cellular automaton (CA) rules, and the evolution of oxygen, drugs and chemokine dynamics are incorporated in order to study the effects of the microenvironment in the pathological lesion. We allow bacteria to switch states depending on oxygen concentration, which affects how they respond to treatment. This is the first multiscale model of its type to consider both oxygen-driven phenotypic switching of the Mycobacterium tuberculosis and antibiotic treatment. Using this model, we investigate the role of bacterial cell state and of initial bacterial location on treatment outcome. We demonstrate that when bacteria are located further away from blood vessels, less favourable outcomes are more likely, i.e. longer time before infection is contained/cleared, treatment failure or later relapse. We also show that in cases where bacteria remain at the end of simulations, the organisms tend to be slower-growing and are often located within granulomas, surrounded by caseous material.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 206628 MEDLINE  
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[PMID]: 29524390
[Au] Autor:Gou W; Zhang Z; Yang C; Li Y
[Ad] Address:PICU, First Hospital of Jilin University, Changchun, Jilin, 130021, China.
[Ti] Title:MiR-223/Pknox1 axis protects mice from CVB3-induced viral myocarditis by modulating macrophage polarization.
[So] Source:Exp Cell Res;, 2018 Mar 07.
[Is] ISSN:1090-2422
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Macrophage polarization plays a crucial role in regulating myocardial inflammation and injuries of coxsackievirus B3 (CVB3)-induced viral myocarditis (VM). It has been reported that miR-223 is a potent regulator of inflammatory responses that involved in macrophage polarization. However, the functional roles of miR-223 in CVB3-induced VM still remain unknown. Here, we found that miR-223 expression was significantly down-regulated in heart tissues and heart-infiltrating macrophages of CVB3-infected mice. Up-regulation of miR-223 in vivo protected the mice against CVB3-induced myocardial injuries characterized by the increased body weight and survival, enhanced left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS), relieved inflammation, depressed creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH) and aspartate transaminase (AST) levels, reduced production of interferon (IFN)-γ, interleukin (IL)-6 as well as increased IL-10. We subsequently found that miR-233 up-regulation significantly suppressed the expression of M1 markers (iNOS, TNF-α and CD 86), and promoted the expression of M2 markers (Arginase-1, Fizz-1 and CD 206) in vivo and in vitro. Furthermore, we confirmed that miR-223 directly targeted Pknox1 to inhibit its expression, and the expression of Pknox1 was inversely correlated with miR-223 expression in heart tissues and heart-infiltrating macrophages of CVB3-infected mice. Gain-of-function analyses indicated that Pknox1 overexpression partially reversed the polarization phenotypes regulated by miR-223 overexpression. Taken together, the data suggest that miR-223 protects against CVB3-induced inflammation and myocardial damage, which may partly attribute to the regulation of macrophage polarization via targeting Pknox1.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 206628 MEDLINE  
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[PMID]: 29515975
[Au] Autor:Wang C; Yu Z; Shi X; Tang X; Wang Y; Wang X; An Y; Li S; Li Y; Wang X; Luan W; Chen Z; Liu M; Yu L
[Ad] Address:Key Laboratory of Zoonoses Research, Ministry of Education, Institute of Zoonosis, First Hospital of Jilin University, College of Veterinary Medicine, Jilin University, Changchun, China.
[Ti] Title:Triclosan Enhances the Clearing of Pathogenic Intracellular or but Disturbs the Intestinal Microbiota through mTOR-Independent Autophagy.
[So] Source:Front Cell Infect Microbiol;8:49, 2018.
[Is] ISSN:2235-2988
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:Triclosan (TCS) is a broad-spectrum antimicrobial agent, whose well-known antibacterial mechanism is inhibiting lipid synthesis. Autophagy, an innate immune response, is an intracellular process that delivers the cargo including pathogens to lysosomes for degradation. In this study, we first demonstrated that TCS induced autophagy in a dose-dependent manner in non-phagocytic cells (HeLa) and in macrophages (Raw264.7) and . The western blot results also revealed that TCS induced autophagy via the AMPK/ULK1 and JNK/ERK/p38 pathways independent of mTOR. The immunofluorescence results indicated that TCS up-regulated the expression of the ubiquitin receptors NDP52 and p62 and strengthened the co-localization of these receptors with Typhimurium ( . typhimurium) or ( ) in infected MΦ cells. In addition, sub-lethal concentrations of TCS enhanced the clearing of the pathogens . typhimurium or in infected MΦ and in corresponding mouse infection models . Specifically, we found that a sub-inhibitory concentration of TCS induced autophagy, leading to an imbalance of the intestinal microflora in mice through the analysis of 16s rRNA Sequencing. Together, these results demonstrated that TCS induced autophagy, which enhanced the killing against pathogenic . typhimurium or within mammal cells but broke the balance of the intestinal microflora.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.3389/fcimb.2018.00049

  8 / 206628 MEDLINE  
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[PMID]: 29507108
[Au] Autor:Sun C; Chen SY
[Ad] Address:Department of Physiology and Pharmacology, University of Georgia, Athens, GA 30602.
[Ti] Title:RGC32 Promotes Bleomycin-Induced Systemic Sclerosis in a Murine Disease Model by Modulating Classically Activated Macrophage Function.
[So] Source:J Immunol;, 2018 Mar 05.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Systemic sclerosis (SSc) is a multisystem autoimmune disorder that is characterized by inflammation and fibrosis in the skin and internal organs. Previous studies indicate that inflammatory cells and cytokines play essential roles in the pathogenesis of SSc; however, the mechanisms that underlie the inflammation-driven development of SSc are not fully understood. In this study, we show that response gene to complement 32 (RGC32) is abundantly expressed in mouse macrophages in the early stage of bleomycin-induced SSc. Importantly, RGC32 is required to induce the inflammatory response during the onset of SSc, because RGC32 deficiency in mice significantly ameliorates skin and lung sclerosis and inhibits the expression of inflammatory mediators inducible NO synthase (iNOS) and IL-1ß in macrophages. RGC32 appears to be a novel regulator for the differentiation of classically activated macrophages (M1 macrophages). IFN-γ and LPS stimulation induces RGC32 expression in primary peritoneal macrophages and bone marrow-derived macrophages. RGC32 deficiency impairs the polarization of M1 macrophages and attenuates iNOS and IL-1ß production. Mechanistically, RGC32 interacts with NF-κB proteins and promotes iNOS and IL-1ß expression by binding to their promoters. Collectively, our data reveal that RGC32 promotes the onset of SSc by regulating the inflammatory response of M1 macrophages, and it may serve as a promising therapeutic target for treating SSc.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher

  9 / 206628 MEDLINE  
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[PMID]: 29506555
[Au] Autor:Liu JF; Wu L; Yang LL; Deng WW; Mao L; Wu H; Zhang WF; Sun ZJ
[Ad] Address:The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory of Oral Biomedicine Ministry of Education, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
[Ti] Title:Blockade of TIM3 relieves immunosuppression through reducing regulatory T cells in head and neck cancer.
[So] Source:J Exp Clin Cancer Res;37(1):44, 2018 Mar 05.
[Is] ISSN:1756-9966
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: T-cell immunoglobulin mucin 3 (TIM3) is a negative immune checkpoint and plays a crucial part in tumor-induced immune suppression. However, the mechanism of TIM3 in regulating immunosuppression in head and neck squamous cell carcinoma (HNSCC) was still not quite clear. METHODS: We carried out the immunohistochemistry staining of HNSCC tissue microarrays. Through quantification of the histoscore, we performed the correlation analysis among the TIM3, Galectin-9, Foxp3, CD68 and CD163. The effects of TIM3 on regulatory T cells (Tregs) and macrophages were detected by utilizing the Tgfbr1/Pten 2cKO HNSCC mouse model. Flow cytometry were used to analysis the percent of Tregs, macrophages and IFN-γ. RESULTS: We demonstrated the close association among TIM3/Galectin-9 pathway, regulatory T cell marker (Foxp3) and macrophage marker (CD68, CD163) in human HNSCC. In the transgenic HNSCC mouse model, blockade of TIM3 by the anti-TIM3 monoclonal antibody induced a reduction of CD4 CD25 Foxp3 Tregs. Meanwhile, the population of TIM3 Tregs was also decreased. However, the population of CD206 macrophages was not significantly declined. The increased IFN-γ production on CD8 T cells in anti-TIM3 treatment mice showed that the antitumor immune response was enhanced through suppression of these negative immune factors. CONCLUSIONS: The present study demonstrated that TIM3 was associated with the immunosuppression in HNSCC. And targeting TIM3 can enhance anti-tumor immune response by decreasing Tregs in HNSCC.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1186/s13046-018-0713-7

  10 / 206628 MEDLINE  
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[PMID]: 29501751
[Au] Autor:Zuliani JP; Gutiérrez JM; Teixeira C
[Ad] Address:Laboratório de Farmacologia, Instituto Butantan, Sao Paulo, Brazil; Laboratório de Imunologia Celular Aplicada à Saúde, Fundação Oswaldo Cruz Rondônia/FIOCRUZ-RO, Porto Velho, RO, Brazil; Dep. Medicina, Universidade Federal de Rondônia, UNIR, Porto Velho, RO, Brazil.
[Ti] Title:Signaling pathways involved in zymosan phagocytosis induced by two secreted phospholipases A isolated from Bothrops asper snake venom in macrophages.
[So] Source:Int J Biol Macromol;113:575-582, 2018 Mar 03.
[Is] ISSN:1879-0003
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Phagocytosis, a process involved in host defense, requires coordination of a variety of signaling reactions. MT-II, a catalytically-inactive Lys49-PLA ¸ and MT-III, an active Asp49-PLA isolated from Bothrops asper snake venom, activate phagocytosis in macrophages. In this study the signal pathways mediating zymosan phagocytosis, focusing in lipidic second messengers, were investigated. Macrophages collected from male Swiss mouse peritoneum were obtained 96h after i.p. injection of thioglycollate. Phagocytosis was evaluated with non-opsonized zymosan in the presence or absence of specific inhibitors. Data showed that both venom PLA s increased phagocytosis. Zileuton, Etoricoxib, PACOCF (5-LO, COX-2 and iPLA inhibitors, respectively), as well as WEB2170 (PAF receptor antagonist) significantly reduced phagocytosis induced by both venom PLA s. However, Indomethacin (COX-1/COX-2 inhibitor) and Montelukast (CysL receptor antagonist) did not affect the toxins-induced phagocytosis. Moreover, while PACOCF3 (iPLA inhibitor), reduced the phagocytosis induced by MT-II and MT-III, AACOCF (cPLA inhibitor) significantly reduced the MT-II, but not MT-III-induced phagocytosis. These data suggest the effect of both sPLA s depends on iPLA and that the effect of MT-II depends on activation of cPLA . COX-2 and 5-LO-derived metabolites as well as PAF are involved in the signaling events required for phagocytosis induced by both venom sPLA s.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher


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