Inflammation and cell signaling最新文献

{"title":"Biphasic modulation of noxious heat sensitivity in sensory neurons by peripheral metabotropic glutamate receptors","authors":"T. Masuoka, T. Ishibashi, M. Nishio","doi":"10.14800/ICS.602","DOIUrl":"https://doi.org/10.14800/ICS.602","url":null,"abstract":"Release of glutamate during inflammation and injury changes sensitivity and transmission efficiency of noxious sensory information via glutamate receptors. We found that activation of metabotropic glutamate receptor type 5 (mGluR5) transiently increased, and then subsequently decreased, noxious heat sensitivity. Similarly, mGluR5 activation in cultured sensory neurons potentiated intracellular calcium elevation mediated by transient receptor potential channel, subfamily V, member 1 (TRPV1), a noxious heat receptor; subsequent cessation of mGluR5 activation depressed intracellular calcium levels. The underlying mechanisms were potentiation of TRPV1 current in the presence of mGluR5 ligands and persistent inhibition of voltage-gated calcium channels (VGCC), even after mGluR5 ligand washout. Thus, mGluR5 biphasically modulates TRPV1-mediated cellular responses in sensory neurons, which contributes to heat hyper- and hypoalgesia. These phenomena may contribute to changes in noxious heat sensitivity during inflammation and healing.","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89538831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interactive roles of gut microbiota and gastrointestinal motility in the development of inflammatory disorders","authors":"Hirofumi Okubo, Yusuke Nakatsu, H. Sakoda, A. Kushiyama, M. Fujishiro, T. Fukushima, Y. Matsunaga, H. Ohno, M. Yoneda, H. Kamata, T. Shinjo, M. Iwashita, F. Nishimura, T. Asano","doi":"10.14800/ICS.643","DOIUrl":"https://doi.org/10.14800/ICS.643","url":null,"abstract":"Gut microbiota play essential roles in host physiology. The gut microbiota both influence and are influenced by gastrointestinal (GI) motility. Disruption of intestinal homeostasis and alterations of the gut microbiota are considered to contribute to the pathogenesis of several disorders. Patients suffering from inflammatory disorders, such as inflammatory bowel disease (IBD) and non-alcoholic steatohepatitis (NASH), reportedly have prolonged orocecal transit times with small intestinal bacterial overgrowth and alterations of gut microbiota. These forms of dysbiosis have been suggested to elicit distinct intestinal immune responses, increased intestinal permeability and bacterial translocation, thereby contributing to the pathogenesis of IBD and/or NASH. In a recent report, we raised the possibility that a drug affecting GI motility might influence gut microbiota and the development of NASH. Thus, we investigated the effects of the gastroprokinetic agent mosapride citrate (MC) using a methionine-choline deficient (MCD) diet-induced NASH rodent model. MC treatment exerted a protective effect against MCD diet-induced GI transit time delay, diminished lactic acid bacteria and colonic inflammation, thereby ameliorating NASH with reduced serum endotoxin and increased glucagon-like peptiede-1. Recently, the correction of dysbiosis employing probiotics or fecal transplantation has been investigated as a therapeutic strategy for IBD and NASH. Given the interactive functions of gut microbiota and mediators of GI motility, there is possibility that altering GI motility also has potential as a therapeutic strategy.","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91166700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of oxidative stress in renal injury related to obesity","authors":"D. Pierine, G. Biondo, V. S. Silva, C. Corrêa","doi":"10.14800/ICS.648","DOIUrl":"https://doi.org/10.14800/ICS.648","url":null,"abstract":"The mechanisms linking obesity to kidney damage are unknown. The kidney is a target organ for lesions caused by AGEs. The receptor of AGEs (RAGE) has proinflammatory stimuli and appears to play a role in the pathogenesis of renal disease. Thus, treatment with antioxidants can be beneficial for the prevention and therapy of oxidative stress and inflammation in the kidneys resulting from obesity.","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87751281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Distinct NF-kB activation pathways engaged by T-cell receptor and co-receptor CD28 on T-cells","authors":"Y. R. Thaker, C. Rudd","doi":"10.14800/ICS.613","DOIUrl":"https://doi.org/10.14800/ICS.613","url":null,"abstract":"The transcription factor nuclear factor-kB (NF-kB) is critical for the induction of inflammatory responses in T-cells, survival and differentiation.  Antigen receptor (TCR) and co-receptor CD28 are the central regulators of NF-kB activation in T-cells. Progress in understanding NF-kB activation in T-cells has occurred over the years with the identification of individual adapters such as ADAP and GRB-2 and enzymes such as PKC-θ that regulate NF-kB.  However, little is known whether the engagement of distinct modules by the TCR and CD28 account for the cooperative effects of the two receptors in activating NF-kB.  In this review, we discuss recent advances in our understanding of NF-kB regulation by TCR and CD28.","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82215113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bioactive compounds in Magnifera indica demonstrates dose-dependent anti- inflammatory effects","authors":"Oluwole Oluwafemi Gabriel","doi":"10.14800/ICS.628","DOIUrl":"https://doi.org/10.14800/ICS.628","url":null,"abstract":"Magnifera indica (MI) is one of the notable medicinal plants use for the treatment of inflammatory diseases in folkloric medicine. Recent studies by present author demonstrated anti-inflammatory effects of Mangifera indica to have dose-dependent effects, pointing out this single effect to be relevant to therapeutics findings. However, as far as we know, Mangifera indica has one or no translational drugs or products already established in clinical trials or pharmaceutical practice. This is rather a concern in drug discovery and optimization, particularly for Magnifera indica plant which has various medicinal efficacies been ascribed to its properties. It has been investigated already that, Mangiferin a very potent bioactive compound found inside extracts of Magnifera indica , being a polyphenolic and a glucosyl xanthone has strong antioxidant and anti-inflammatory properties. Various effects like antibacterial, antipyretic, anti diarrhoeal, anti allergic, immunomodulation, anti microbial, gastroprotective have also been ascribed to medicinal use of Mangifera indica . Other phytochemistry found in Mangifera indica includes; Saponin, tannins, steroids, flavoniod, alkaloids, cardiac glycosides, reducing sugar and anthraquinone. All these have been seen to be useful in herbal medicine and cosmetics. Thus, this paper focus on the need to encourage the lead optimization and to adequately promote further research that will formulate bioactive compounds in Magnifera indica for the purpose of treating inflammatory diseases, and the need to conduct more clinical trials using Mangifera indica bioactive compounds for variety of conditions in human volunteers.","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91418442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect and mechanism of BET bromodomain inhibition in macrophage transcriptional programming","authors":"Y. Qiao, L. Ivashkiv","doi":"10.14800/ICS.600","DOIUrl":"https://doi.org/10.14800/ICS.600","url":null,"abstract":"Epigenetic regulation is at the center of gene transcriptional activity, and the epigenetic mechanisms in immune responses have gained increasing attention because of their potential as therapeutic targets. Bromodomain and extra terminal ( BET ) proteins are known to play important roles in transcriptional elongation; disruption of the interaction of BET proteins with acetylated histones suppresses BET-mediated transcription. BET inhibitors have been tested in multiple mouse models as a promising approach to treat various diseases. A recent study addressed the therapeutic potential of a BET inhibitor I-BET151 by assessing its effect on human monocyte and macrophage responses. The study focused on the interference of I-BET151 with cytokine-stimulated JAK-STAT pathways that are important for monocyte polarization and inflammatory responses. In both pro-inflammatory and alternative macrophage responses, I-BET151 exhibited differential repression of cytokine target genes and the repression was independent of protein synthesis. The study also found that I-BET151 repressed TLR4- and TNF-induced interferon responses by diminishing both autocrine IFN-b expression and IFN-b-induced transcription. Further investigation of interferon responses showed that I-BET151 administration did not affect JAK-STAT activation or STAT1 recruitment to target promoters, but instead blocked  RNA polymerase II recruitment to gene proximal promoters as well as distal regulatory regions. These findings expand the understanding of the effect and therapeutic potential of BET protein inhibition in inflammatory diseases.","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90704330","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fecal calprotectin: a biomarker for intestinal inflammation","authors":"G. P. Caviglia, G. Touscoz, R. Pellicano, M. Astegiano","doi":"10.14800/ICS.563","DOIUrl":"https://doi.org/10.14800/ICS.563","url":null,"abstract":"In the clinical setting may be difficult the discrimination of patients with inflammatory bowel diseases from those with functional intestinal disorders due to the overlapping and non-specific symptoms, such as abdominal pain and altered bowel habit. Several blood markers currently help clinicians in the management of these patients, but the low specificity makes them unreliable for the detection and monitoring of the disease activity. The gold standard to establish a diagnosis of organic bowel disease is colonoscopy with multiple biopsies, but is an invasive and costly procedure. In the last decade, fecal calprotectin (FC), a cytosolic protein mainly found in neutrophil granulocytes, has been proposed as a surrogate marker of intestinal mucosa inflammation and has been associated with several gastrointestinal disorders. We recently addressed FC ability in distinguish inflammatory from functional disorders, taking into consideration different pathological intestinal conditions. In this research highlight we provide a brief review on FC role as a biomarker of intestinal inflammation discussing the clinical applications.","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76361053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent studies on anti-inflammatory effects of radon inhalation in mice","authors":"Norie Kanzaki, T. Kataoka, Reo Etani, K. Yamaoka","doi":"10.14800/ICS.601","DOIUrl":"https://doi.org/10.14800/ICS.601","url":null,"abstract":"Radon therapy, which has been performed in Misasa (Japan) and Badgastein (Austria), was found to have a beneficial effect on pain-related diseases. Although several clinical studies of the curative effects on pain related diseases have been reported, the mechanism remains to be incompletely elucidated. In order to further clarify the mechanism, we developed radon exposure systems for small animals. In the present paper, we review several studies on the anti-inflammatory effects of radon inhalation in mice. We first examined whether radon inhalation inhibits carrageenan-induced inflammatory paw in mice. Radon concentration in mouse cage was approximately 2000 Bq/m 3 , which is similar to the level of radon therapy at Misasa Medical Center, Okayama University Hospital. Although carrageenan administration into right hind paw of mice induced paw edema, radon inhalation inhibited the edema. Antioxidants such as superoxide dismutase (SOD) and catalase were significantly higher in the radon-treated mice than in the sham-treated mice. Since the development of carrageenan-induced inflammation is mediated by reactive oxygen species (ROS), the inhibition of paw edema by radon inhalation is probably due to activation of antioxidant functions. We next examined the effects of radon inhalation on dextran sulfate sodium (DSS)-induced colitis in mice. Results showed that radon inhalation suppressed the damage caused by DSS-induced colitis. In addition, the mediators of inflammatory response such as tumor necrosis factor-alpha (TNF-α) were inhibited, and antioxidants such as SOD were increased by radon inhalation. Next, we examined the effects of radon inhalation on formalin-induced inflammatory pain in mice. Results showed that radon inhalation inhibited the licking response time. TNF-α, activated by formalin-induced inflammation, was lower in the radon-treated mice than in the sham-treated mice. Antioxidant activities such as SOD activity were increased in the mice that inhaled radon. These findings suggested that radon inhalation inhibits several types of inflammation in mice due to activation of antioxidant functions.","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75469349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of nestin-associated genes in the inner ear of newborn rats following injury and hypoxia","authors":"J. Gross, H. Olze, B. Mazurek","doi":"10.14800/ICS.549","DOIUrl":"https://doi.org/10.14800/ICS.549","url":null,"abstract":"We used organotypic cultures of the stria vascularis (SV), the organ of Corti (OC) and the modiolus (MOD) of newborn rats to analyze the differential expression levels and responses of cytoskeletal, myelin- and neural growth factor-associated genes following preparatory injury and hypoxia. The transcript mRNA levels of the neurofilaments Nefl , Nefm, the microtubule-associated proteins Mapt, Map1a, Map2, and of the myelin basic protein Mbp decrease during 24 h in a coordinated way across the MOD and OC regions. The increased cell death rate in the MOD region is associated with an increased expression of Nes, the transcript encoding the intermediate filament nestin, and of the neural growth factor receptor Ngfr, the growth-associated protein 43 Gap43 and the Purkinje cell protein Pcp4. The correlation analysis revealed close associations between Nes expression and genes involved in apoptotic and necrotic cell death (caspase Casp3, calpains Capn1, Capn2, Capns1), the glutamate pathway (glutamate receptor NMDA associated protein 1 Grina, glial high affinity glutamate transporter Slc1a3), cytoskeletal genes (Nefm, Map2, Map1a, Mbp), transcription factors (hypoxia inducible factor Hif-1a, jun proto-oncogene Jun, brain expressed myelocytomatosis B-myc, HES family bHLH transcription factor 1 Hes-1, forkhead-box D3 Foxd3) and neural growth factors ( Ngfr, Gap43 and Pcp4 ) . The unique response and the composition of the Nes cluster made us conclude that the expression of cell-death-associated genes and the regeneration-associated genes takes place in a coordinated way, and differs between the MOD and the OC/SV regions.","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77652638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Asynchronous inflammation and myogenic cell migration limit muscle tissue regeneration mediated by a cellular scaffolds.","authors":"K. Garg, C. Ward, B. Corona","doi":"10.14800/ICS.530","DOIUrl":"https://doi.org/10.14800/ICS.530","url":null,"abstract":"Volumetric muscle loss (VML) following orthopaedic trauma results in chronic loss of strength and can contribute to disability. Tissue engineering and regenerative medicine approaches to regenerate the lost skeletal muscle and improve functional outcomes are currently under development. At the forefront of these efforts, decellularized extracellular matrices (ECMs) have reached clinical testing and provide the foundation for other approaches that include stem/progenitor cell delivery. ECMs have been demonstrated to possess many qualities to initiate regeneration, to include stem cell chemotaxis and pro-regenerative macrophage polarization. However, the majority of observations indicate that ECM-repair of VML does not promote appreciable muscle fiber regeneration. In a recent study, ECM-repair of VML was compared to classical muscle fiber regeneration (Garg et al., 2014, Cell & Tissue Research) mediated by autologous minced grafts. The most salient findings of this study were: 1) Satellite cells did not migrate into the scaffold beyond ~0.5 mm from the remaining host tissue, although other migratory stem cells (Sca-1+) were observed throughout the scaffold;2) Macrophage migration to the scaffold was over two-times that observed with muscle grafts, but they appeared to be less active, as gene expression of pro- and anti-inflammatory cytokines (TNF-α, IL-12, IL-4, IL-10, VEGF, and TGF-β1) was significantly reduced in scaffold-repaired muscles; And, 3) scaffolds did not promote appreciable muscle fiber regeneration. Collectively, these data suggest that the events following ECM transplantation in VML are either incongruous or asynchronous with classical muscle fiber regeneration.","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82921699","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}