The Experts below are selected from a list of 177 Experts worldwide ranked by ideXlab platform
Artur Schmidtchen - One of the best experts on this subject based on the ideXlab platform.
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Toll-like Receptor 3 Agonist, Polyinosinic-Polycytidylic Acid, Upregulates Carbonic Anhydrase II in Human Keratinocytes.
Acta Dermato-venereologica, 2018Co-Authors: Bani Kaur Suri, Navin Kumar Verma, Artur SchmidtchenAbstract:Carbonic anhydrases are ubiquitously expressed enzymes that reversibly hydrate carbon dioxide to bicar-bonate and protons. While the main function of carbonic anhydrases is to regulate pH and osmotic balance, their involvement in other physiological processes remains to be explored. This study analysed changes in mRNA and protein levels of carbonic anhydrase II in human primary keratinocytes treated with various toll-like receptor agonists and cytokines. A significant upregulation of carbonic anhydrase II at the mRNA and protein levels was observed upon treatment with polyinosinic-Polycytidylic Acid, a toll-like receptor 3 agonist. Furthermore, in agreement with the increased expression of carbonic anhydrase II in atopic dermatitis skin, carbonic anhydrase II was upregulated by the Th2 cytokines interleukins-4 and-13. In conclusion, these results suggest a potential role of carbonic anhydrase II in Th2-dependent and toll-like receptor 3-induced pathways in inflammatory skin conditions. (Less)
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Toll-like Receptor 3 Agonist, Polyinosinic-Polycytidylic Acid, Upregulates Carbonic Anhydrase II in Human Keratinocytes.
Acta dermato-venereologica, 2018Co-Authors: Bani Kaur Suri, Navin Kumar Verma, Artur SchmidtchenAbstract:Carbonic anhydrases are ubiquitously expressed enzymes that reversibly hydrate carbon dioxide to bicarbonate and protons. While the main function of carbonic anhydrases is to regulate pH and osmotic balance, their involvement in other physiological processes remains to be explored. This study analysed changes in mRNA and protein levels of carbonic anhydrase II in human primary keratinocytes treated with various toll-like receptor agonists and cytokines. A significant upregulation of carbonic anhydrase II at the mRNA and protein levels was observed upon treatment with polyinosinic-Polycytidylic Acid, a toll-like receptor 3 agonist. Furthermore, in agreement with the increased expression of carbonic anhydrase II in atopic dermatitis skin, carbonic anhydrase II was upregulated by the Th2 cytokines interleukins -4 and -13. In conclusion, these results suggest a potential role of carbonic anhydrase II in Th2-dependent and toll-like receptor 3-induced pathways in inflammatory skin conditions.
Bani Kaur Suri - One of the best experts on this subject based on the ideXlab platform.
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Toll-like Receptor 3 Agonist, Polyinosinic-Polycytidylic Acid, Upregulates Carbonic Anhydrase II in Human Keratinocytes.
Acta Dermato-venereologica, 2018Co-Authors: Bani Kaur Suri, Navin Kumar Verma, Artur SchmidtchenAbstract:Carbonic anhydrases are ubiquitously expressed enzymes that reversibly hydrate carbon dioxide to bicar-bonate and protons. While the main function of carbonic anhydrases is to regulate pH and osmotic balance, their involvement in other physiological processes remains to be explored. This study analysed changes in mRNA and protein levels of carbonic anhydrase II in human primary keratinocytes treated with various toll-like receptor agonists and cytokines. A significant upregulation of carbonic anhydrase II at the mRNA and protein levels was observed upon treatment with polyinosinic-Polycytidylic Acid, a toll-like receptor 3 agonist. Furthermore, in agreement with the increased expression of carbonic anhydrase II in atopic dermatitis skin, carbonic anhydrase II was upregulated by the Th2 cytokines interleukins-4 and-13. In conclusion, these results suggest a potential role of carbonic anhydrase II in Th2-dependent and toll-like receptor 3-induced pathways in inflammatory skin conditions. (Less)
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Toll-like Receptor 3 Agonist, Polyinosinic-Polycytidylic Acid, Upregulates Carbonic Anhydrase II in Human Keratinocytes.
Acta dermato-venereologica, 2018Co-Authors: Bani Kaur Suri, Navin Kumar Verma, Artur SchmidtchenAbstract:Carbonic anhydrases are ubiquitously expressed enzymes that reversibly hydrate carbon dioxide to bicarbonate and protons. While the main function of carbonic anhydrases is to regulate pH and osmotic balance, their involvement in other physiological processes remains to be explored. This study analysed changes in mRNA and protein levels of carbonic anhydrase II in human primary keratinocytes treated with various toll-like receptor agonists and cytokines. A significant upregulation of carbonic anhydrase II at the mRNA and protein levels was observed upon treatment with polyinosinic-Polycytidylic Acid, a toll-like receptor 3 agonist. Furthermore, in agreement with the increased expression of carbonic anhydrase II in atopic dermatitis skin, carbonic anhydrase II was upregulated by the Th2 cytokines interleukins -4 and -13. In conclusion, these results suggest a potential role of carbonic anhydrase II in Th2-dependent and toll-like receptor 3-induced pathways in inflammatory skin conditions.
Wan Su Park - One of the best experts on this subject based on the ideXlab platform.
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Anti-Inflammatory Effect of Baicalein on Polyinosinic–Polycytidylic Acid-Induced RAW 264.7 Mouse Macrophages
Viruses, 2018Co-Authors: Young Jin Kim, Ji-young Lee, Hyun-ju Kim, Do-hoon Kim, Mi Suk Kang, Wan Su ParkAbstract:Baicalein (3,3′,4′,5,6-pentahydroxyflavone) is a well-known antioxidant found in many plants, such as in the roots of Scutellaria baicalensis. In this study, we evaluate the inhibitory effect of baicalein on the inflammatory cascade in RAW 264.7 mouse macrophages induced by viral-like material. Experimental assays used in this study included Griess reagent assay for nitric oxide (NO) production, Fluo-4 assay for intracellular calcium release, multiplex cytokine assay, and quantitative real time RT-PCR assay. To induce inflammation, RAW 264.7 cells were treated with polyinosinic–Polycytidylic Acid (poly I:C), a synthetic analog of double-stranded RNA (dsRNA). Baicalein at concentrations up to 100 μM significantly inhibited the production of NO, IL-1α, IL-6, G-CSF, GM-CSF, VEGF, MCP-1, IP-10, LIX, and RANTES as well as calcium release in RAW 264.7 cells induced by poly I:C (50 µg/mL) (all p < 0.05). Baicalein at concentrations up to 50 μM also significantly inhibited mRNA expression of STAT1, STAT3, CHOP, and Fas in poly I:C-induced RAW 264.7 cells (p < 0.05). In conclusion, baicalein has anti-inflammatory effect in double-stranded RNA (dsRNA)-induced macrophages by inhibiting NO, cytokines, chemokines, and growth factors via the endoplasmic reticulum stress–CHOP/STAT pathway.
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Anti-Inflammatory Effect of Quercetin on RAW 264.7 Mouse Macrophages Induced with Polyinosinic-Polycytidylic Acid.
Molecules (Basel Switzerland), 2016Co-Authors: Young Jin Kim, Wan Su ParkAbstract:Wogonin (5,7-dihydroxy-8-methoxyflavone) is an active flavonoid compound originally isolated from Scutellaria radix, which has been used to treat lung inflammation in Korea, China, and Japan. Wogonin has been known to inhibit inducible nitric oxide synthase and have the anti-tumor properties. However, the effects of wogonin on virus-induced macrophages are not fully reported. In this study, the anti-inflammatory effect of wogonin on double-stranded RNA (dsRNA)-induced macrophages was examined. Wogonin restored the cell viability in dsRNA [polyinosinic-Polycytidylic Acid]-induced RAW 264.7 mouse macrophages at concentrations of up to 50 μM. Wogonin significantly inhibited the production of nitric oxide, IL-1α, IL-1β, IL-6, IL-10, IP-10, G-CSF, GM-CSF, LIF (IL-6 class cytokine), LIX/CXCL5, MCP-1, M-CSF, MIP-1α, MIP-1β, MIP-2, RANTES/CCL5, TNF-α, and VEGF as well as calcium release and mRNA expression of signal transducer and activated transcription 1 (STAT1) and STAT3 in dsRNA-induced RAW 264.7 cells (P < 0.05). In conclusion, wogonin has anti-inflammatory properties related with its inhibition of nitric oxide, cytokines, chemokines, and growth factors in dsRNA-induced macrophages via the calcium-STAT pathway.
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Anti-inflammatory effect of chrysin on RAW 264.7 mouse macrophages induced with polyinosinic-Polycytidylic Acid
Biotechnology and Bioprocess Engineering, 2015Co-Authors: Wan Su ParkAbstract:Chrysin (5,7-Dihydroxyflavone) is an active flavonoid isolated from Scutellariae Radix which has been used to treat pneumonia, laryngopharyngitis, jaundice, shigellosis, and breast mass in Korea, China, and Japan. Chrysin has been already reported to inhibit inducible nitric oxide synthase and cyclooxygenase-2 in lipopolysaccharideinduced macrophages. However, the effect of chrysin on virus-induced macrophages is not fully reported. In this study, the anti-inflammatory effect of chrysin on doublestranded RNA (dsRNA)-induced macrophages was examined. Production of Nitric oxide (NO), various cytokines, as well as calcium release and mRNA expression of CHOP and Fas in dsRNA [polyinosinic-Polycytidylic Acid]-induced RAW 264.7 mouse macrophages were evaluated. Chrysin restored the cell viability in dsRNA [polyinosinicPolycytidylic Acid]-induced RAW 264.7 mouse macrophages at concentrations of up to 50 μM. Chrysin significantly inhibited the production of NO, IL-1α, IL-1β, IL-6, IL-10, IP-10, G-CSF, GM-CSF, LIF, LIX/CXCL5, MCP-1, MCSF, MIP-1α, MIP-1β, MIP-2, RANTES, TNF-α, and VEGF as well as calcium release and mRNA expression of CHOP and Fas in dsRNA [polyinosinic-Polycytidylic Acid]-induced RAW 264.7 mouse macrophages ( P < 0.05). These data suggest that chrysin has anti-inflammatory properties related with its inhibition of nitric oxide, cytokines, chemokines, and growth factors in dsRNA-induced macrophages via the ER stress-CHOP pathway.
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Anti-Inflammatory Effect of Quercetin on RAW 264.7 Mouse Macrophages Induced with Polyinosinic-Polycytidylic Acid
Proceedings of 1st Electronic Conference on Molecular Science, 2015Co-Authors: Young Jin Kim, Wan Su ParkAbstract:Quercetin (3,3′,4′,5,6-Pentahydroxyflavone) is one of well-known antioxidants and a flavonol found in many fruits, leaves, and vegetables. Quercetin is also well-known to have anti-inflammatory effects on lipopolysaccharide-induced macrophages. However, the effects of quercetin on virus-induced macrophages are not fully reported. In this study, the anti-inflammatory effect of quercetin on double-stranded RNA (dsRNA)-induced macrophages was examined. Quercetin at concentrations of up to 50 μM significantly inhibited the production of nitric oxide (NO), IL-6, MCP-1, IP-10, RANTES, GM-CSF, G-CSF, TNF-α, LIX,VEGF, and MIP-1α as well as calcium release in dsRNA [50 µg/mL of polyinosinic-Polycytidylic Acid]-induced RAW 264.7 mouse macrophages (P < 0.05). Quercetin at concentrations of up to 50 μM also significantly inhibited mRNA expression of signal transducer and activated transcription 1 (STAT1) and STAT3 in dsRNA-induced RAW 264.7 (P < 0.05). In conclusion, quercetin has alleviating effects on viral inflammation concerned with its inhibition of NO, cytokines, chemokines, and growth factors in dsRNA-induced macrophages via the calcium-STAT pathway.
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anti inflammatory effect of quercetin on raw 264 7 mouse macrophages induced with polyinosinic Polycytidylic Acid
Molecules, 2015Co-Authors: Young Jin Kim, Wan Su ParkAbstract:Quercetin (3,3',4',5,6-pentahydroxyflavone) is a well-known antioxidant and a flavonol found in many fruits, leaves, and vegetables. Quercetin also has known anti-inflammatory effects on lipopolysaccharide-induced macrophages. However, the effects of quercetin on virus-induced macrophages have not been fully reported. In this study, the anti-inflammatory effect of quercetin on double-stranded RNA (dsRNA)-induced macrophages was examined. Quercetin at concentrations up to 50 μM significantly inhibited the production of NO, IL-6, MCP-1, IP-10, RANTES, GM-CSF, G-CSF, TNF-α, LIF, LIX, and VEGF as well as calcium release in dsRNA (50 μg/mL of polyinosinic-Polycytidylic Acid)-induced RAW 264.7 mouse macrophages (p < 0.05). Quercetin at concentrations up to 50 μM also significantly inhibited mRNA expression of signal transducer and activated transcription 1 (STAT1) and STAT3 in dsRNA-induced RAW 264.7 cells (p < 0.05). In conclusion, quercetin had alleviating effects on viral inflammation based on inhibition of NO, cytokines, chemokines, and growth factors in dsRNA-induced macrophages via the calcium-STAT pathway.
Adelheid Elbeburger - One of the best experts on this subject based on the ideXlab platform.
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epicutaneous administration of the pattern recognition receptor agonist polyinosinic Polycytidylic Acid activates the mda5 mavs pathway in langerhans cells
The FASEB Journal, 2018Co-Authors: Pooja Tajpara, Christopher Schuster, Elisabeth Schön, Philip Kienzl, Martin Vierhapper, Michael Mildner, Adelheid ElbeburgerAbstract:Together with keratinocytes (KCs) and the dense network of Langerhans cells (LCs), the epidermis is an ideal portal for vaccine delivery. Pattern recognition receptor agonists, in particular polyinosinic-Polycytidylic Acid [p(I:C)], are promising adjuvant candidates for therapeutic vaccination to generate protective T-cell immunity. Here we established an ex vivo skin explant model to study the expression and activation of double-stranded RNA (dsRNA)-sensing pattern recognition receptors in LCs and KCs in human skin. Whereas KCs expressed all known dsRNA sensing receptors at a constitutive and inducible level, LCs exclusively expressed melanoma differentiation-associated protein 5 (MDA5) in untreated skin and freshly isolated cells. Comparative assessments of downstream signaling pathways induced by p(I:C) revealed distinct mitochondrial antiviral-signaling protein, IFN-regulatory factor 3, and NF-κB activation in LCs and KCs. Consequently, p(I:C) treatment of LCs significantly induced IFN-α and IFN-β mRNA expression, while in KCs an up-regulation of IFN-β and TNF-α mRNA was detectable. Stimulation of LCs with specific ligands revealed that not the TLR3- but only the MDA5-specific ligand induced IFN-α2, IFN-β, and TNF-α cytokines, but no IL-6 and -8. In KCs, both ligands induced production of high IL-6 and IL-8 levels, and low IFN-α2 and IFN-β levels, indicating that different dsRNA-sensing receptors and/or downstream signaling pathways are activated in both cell types. Our data suggest that MDA5 may be an attractive adjuvant target for epicutaneous delivery of therapeutic vaccines with the goal to target LCs.-Tajpara, P., Schuster, C., Schon, E., Kienzl, P., Vierhapper, M., Mildner, M., Elbe-Burger, A. Epicutaneous administration of the pattern recognition receptor agonist polyinosinic-Polycytidylic Acid activates the MDA5/MAVS pathway in Langerhans cells.
Tsukasa Seya - One of the best experts on this subject based on the ideXlab platform.
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inam plays a critical role in ifn γ production by nk cells interacting with polyinosinic Polycytidylic Acid stimulated accessory cells
Journal of Immunology, 2014Co-Authors: Jun Kasamatsu, Masahiro Azuma, Hiroyuki Oshiumi, Yuka Morioka, Masaru Okabe, Takashi Ebihara, Misako Matsumoto, Tsukasa SeyaAbstract:Polyinosinic-Polycytidylic Acid strongly promotes the antitumor activity of NK cells via TLR3/Toll/IL-1R domain–containing adaptor molecule 1 and melanoma differentiation-associated protein-5/mitochondrial antiviral signaling protein pathways. Polyinosinic-Polycytidylic Acid acts on accessory cells such as dendritic cells (DCs) and macrophages (Mφs) to secondarily activate NK cells. In a previous study in this context, we identified a novel NK-activating molecule, named IFN regulatory factor 3–dependent NK-activating molecule (INAM), a tetraspanin-like membrane glycoprotein (also called Fam26F). In the current study, we generated INAM-deficient mice and investigated the in vivo function of INAM. We found that cytotoxicity against NK cell–sensitive tumor cell lines was barely decreased in Inam −/− mice, whereas the number of IFN-γ–producing cells was markedly decreased in the early phase. Notably, deficiency of INAM in NK and accessory cells, such as CD8α + conventional DCs and Mφs, led to a robust decrease in IFN-γ production. In conformity with this phenotype, INAM effectively suppressed lung metastasis of B16F10 melanoma cells, which is controlled by NK1.1 + cells and IFN-γ. These results suggest that INAM plays a critical role in NK-CD8α + conventional DC (and Mφ) interaction leading to IFN-γ production from NK cells in vivo. INAM could therefore be a novel target molecule for cancer immunotherapy against IFN-γ–suppressible metastasis.
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INAM Plays a Critical Role in IFN-γ Production by NK Cells Interacting with Polyinosinic-Polycytidylic Acid–Stimulated Accessory Cells
Journal of immunology (Baltimore Md. : 1950), 2014Co-Authors: Jun Kasamatsu, Masahiro Azuma, Hiroyuki Oshiumi, Yuka Morioka, Masaru Okabe, Takashi Ebihara, Misako Matsumoto, Tsukasa SeyaAbstract:Polyinosinic-Polycytidylic Acid strongly promotes the antitumor activity of NK cells via TLR3/Toll/IL-1R domain–containing adaptor molecule 1 and melanoma differentiation-associated protein-5/mitochondrial antiviral signaling protein pathways. Polyinosinic-Polycytidylic Acid acts on accessory cells such as dendritic cells (DCs) and macrophages (Mφs) to secondarily activate NK cells. In a previous study in this context, we identified a novel NK-activating molecule, named IFN regulatory factor 3–dependent NK-activating molecule (INAM), a tetraspanin-like membrane glycoprotein (also called Fam26F). In the current study, we generated INAM-deficient mice and investigated the in vivo function of INAM. We found that cytotoxicity against NK cell–sensitive tumor cell lines was barely decreased in Inam −/− mice, whereas the number of IFN-γ–producing cells was markedly decreased in the early phase. Notably, deficiency of INAM in NK and accessory cells, such as CD8α + conventional DCs and Mφs, led to a robust decrease in IFN-γ production. In conformity with this phenotype, INAM effectively suppressed lung metastasis of B16F10 melanoma cells, which is controlled by NK1.1 + cells and IFN-γ. These results suggest that INAM plays a critical role in NK-CD8α + conventional DC (and Mφ) interaction leading to IFN-γ production from NK cells in vivo. INAM could therefore be a novel target molecule for cancer immunotherapy against IFN-γ–suppressible metastasis.
