The Experts below are selected from a list of 321 Experts worldwide ranked by ideXlab platform
Stefan Fichtnerfeigl - One of the best experts on this subject based on the ideXlab platform.
-
induction of il 13 triggers tgf β1 dependent tissue fibrosis in chronic 2 4 6 Trinitrobenzene sulfonic acid colitis
Journal of Immunology, 2007Co-Authors: Stefan Fichtnerfeigl, Ivan J Fuss, Cheryl A Young, Tomohiro Watanabe, Edward K Geissler, Hansjiirgen Schlitt, Atsushi Kitani, Warren StroberAbstract:To investigate the immunopathogenesis of inflammation-associated fibrosis, we analyzed the chronic colitis and late-developing fibrosis occurring in BALB/c mice administered weekly doses of intrarectal 2,4,6-Trinitrobenzene sulfonic acid. We showed first in this model that an initial Th1 response involving IL-12p70 and IFN-γ subsides after 3 wk to be supplanted by an IL-23/IL-25 response beginning after 4–5 wk. This evolution is followed by gradually increasing production of IL-17 and cytokines ordinarily seen in a Th2 response, particularly IL-13, which reaches a plateau at 8–9 wk. In vitro stimulation studies suggest that this IL-13 production is dependent on IL-23 and IL-25, but not on IL-12p70. We then show that IL-13 production results in the induction of an IL-13R formerly thought to function only as a decoy receptor, IL-13Rα2, and this receptor is critical to the production of TGF-β1 and the onset of fibrosis. Thus, if IL-13 signaling through this receptor is blocked by administration of soluble IL-13Rα2-Fc, or by administration of IL-13Rα2-specific small interfering RNA, TGF-β1 is not produced and fibrosis does not occur. These studies show that in chronic 2,4,6-Trinitrobenzene sulfonic acid colitis, fibrosis is dependent on the development of an IL-13 response that acts through a novel cell surface-expressed IL-13R to induce TGF-β1. A similar mechanism may obtain in certain forms of human inflammatory bowel disease.
-
induction of il 13 triggers tgf β1 dependent tissue fibrosis in chronic 2 4 6 Trinitrobenzene sulfonic acid colitis
Journal of Immunology, 2007Co-Authors: Stefan Fichtnerfeigl, Ivan J Fuss, Cheryl A Young, Tomohiro Watanabe, Edward K Geissler, Hansjiirgen Schlitt, Atsushi Kitani, Warren StroberAbstract:To investigate the immunopathogenesis of inflammation-associated fibrosis, we analyzed the chronic colitis and late-developing fibrosis occurring in BALB/c mice administered weekly doses of intrarectal 2,4,6-Trinitrobenzene sulfonic acid. We showed first in this model that an initial Th1 response involving IL-12p70 and IFN-gamma subsides after 3 wk to be supplanted by an IL-23/IL-25 response beginning after 4-5 wk. This evolution is followed by gradually increasing production of IL-17 and cytokines ordinarily seen in a Th2 response, particularly IL-13, which reaches a plateau at 8-9 wk. In vitro stimulation studies suggest that this IL-13 production is dependent on IL-23 and IL-25, but not on IL-12p70. We then show that IL-13 production results in the induction of an IL-13R formerly thought to function only as a decoy receptor, IL-13Ralpha(2), and this receptor is critical to the production of TGF-beta(1) and the onset of fibrosis. Thus, if IL-13 signaling through this receptor is blocked by administration of soluble IL-13Ralpha(2)-Fc, or by administration of IL-13Ralpha(2)-specific small interfering RNA, TGF-beta(1) is not produced and fibrosis does not occur. These studies show that in chronic 2,4,6-Trinitrobenzene sulfonic acid colitis, fibrosis is dependent on the development of an IL-13 response that acts through a novel cell surface-expressed IL-13R to induce TGF-beta(1). A similar mechanism may obtain in certain forms of human inflammatory bowel disease.
Warren Strober - One of the best experts on this subject based on the ideXlab platform.
-
induction of il 13 triggers tgf β1 dependent tissue fibrosis in chronic 2 4 6 Trinitrobenzene sulfonic acid colitis
Journal of Immunology, 2007Co-Authors: Stefan Fichtnerfeigl, Ivan J Fuss, Cheryl A Young, Tomohiro Watanabe, Edward K Geissler, Hansjiirgen Schlitt, Atsushi Kitani, Warren StroberAbstract:To investigate the immunopathogenesis of inflammation-associated fibrosis, we analyzed the chronic colitis and late-developing fibrosis occurring in BALB/c mice administered weekly doses of intrarectal 2,4,6-Trinitrobenzene sulfonic acid. We showed first in this model that an initial Th1 response involving IL-12p70 and IFN-γ subsides after 3 wk to be supplanted by an IL-23/IL-25 response beginning after 4–5 wk. This evolution is followed by gradually increasing production of IL-17 and cytokines ordinarily seen in a Th2 response, particularly IL-13, which reaches a plateau at 8–9 wk. In vitro stimulation studies suggest that this IL-13 production is dependent on IL-23 and IL-25, but not on IL-12p70. We then show that IL-13 production results in the induction of an IL-13R formerly thought to function only as a decoy receptor, IL-13Rα2, and this receptor is critical to the production of TGF-β1 and the onset of fibrosis. Thus, if IL-13 signaling through this receptor is blocked by administration of soluble IL-13Rα2-Fc, or by administration of IL-13Rα2-specific small interfering RNA, TGF-β1 is not produced and fibrosis does not occur. These studies show that in chronic 2,4,6-Trinitrobenzene sulfonic acid colitis, fibrosis is dependent on the development of an IL-13 response that acts through a novel cell surface-expressed IL-13R to induce TGF-β1. A similar mechanism may obtain in certain forms of human inflammatory bowel disease.
-
induction of il 13 triggers tgf β1 dependent tissue fibrosis in chronic 2 4 6 Trinitrobenzene sulfonic acid colitis
Journal of Immunology, 2007Co-Authors: Stefan Fichtnerfeigl, Ivan J Fuss, Cheryl A Young, Tomohiro Watanabe, Edward K Geissler, Hansjiirgen Schlitt, Atsushi Kitani, Warren StroberAbstract:To investigate the immunopathogenesis of inflammation-associated fibrosis, we analyzed the chronic colitis and late-developing fibrosis occurring in BALB/c mice administered weekly doses of intrarectal 2,4,6-Trinitrobenzene sulfonic acid. We showed first in this model that an initial Th1 response involving IL-12p70 and IFN-gamma subsides after 3 wk to be supplanted by an IL-23/IL-25 response beginning after 4-5 wk. This evolution is followed by gradually increasing production of IL-17 and cytokines ordinarily seen in a Th2 response, particularly IL-13, which reaches a plateau at 8-9 wk. In vitro stimulation studies suggest that this IL-13 production is dependent on IL-23 and IL-25, but not on IL-12p70. We then show that IL-13 production results in the induction of an IL-13R formerly thought to function only as a decoy receptor, IL-13Ralpha(2), and this receptor is critical to the production of TGF-beta(1) and the onset of fibrosis. Thus, if IL-13 signaling through this receptor is blocked by administration of soluble IL-13Ralpha(2)-Fc, or by administration of IL-13Ralpha(2)-specific small interfering RNA, TGF-beta(1) is not produced and fibrosis does not occur. These studies show that in chronic 2,4,6-Trinitrobenzene sulfonic acid colitis, fibrosis is dependent on the development of an IL-13 response that acts through a novel cell surface-expressed IL-13R to induce TGF-beta(1). A similar mechanism may obtain in certain forms of human inflammatory bowel disease.
-
probiotics ameliorate recurrent th1 mediated murine colitis by inducing il 10 and il 10 dependent tgf β bearing regulatory cells
Journal of Immunology, 2005Co-Authors: Claudia Di Giacinto, Warren Strober, Mariarosaria Marinaro, Massimo Sanchez, Monica BoirivantAbstract:Recent studies of murine models of mucosal inflammation suggest that, whereas some kinds of bacterial microflora are inducers of disease, others, known as probiotics, prevent disease. In the present study, we analyzed the regulatory cytokine and cell response to probiotic (VSL#3) administration in the context of the Th1 T cell colitis induced by Trinitrobenzene sulfonic acid treatment of SJL/J mice. Daily administration of probiotics for 3 wk to mice during a remission period between a first and second course of colitis induced by Trinitrobenzene sulfonic acid, resulted in a milder form of recurrent colitis than observed in mice administered PBS during this same period. This protective effect was attributable to effects on the lamina propria mononuclear cell (LPMC) population, because it could be transferred by LPMC from probiotic-treated mice to naive mice. Probiotic administration was associated with an early increase in the production of IL-10 and an increased number of regulatory CD4+ T cells bearing surface TGF-β in the form of latency-associated protein (LAP) (LAP+ T cells). The latter were dependent on the IL-10 production because administration of anti-IL-10R mAb blocked their appearance. Finally, the LAP+ T cells were essential to the protective effect of probiotics because administration of anti-IL-10R or anti-TGF-β at the initiation of recurrent colitis induction or depletion of LAP+ T cells from LPMC abolished the latter’s capacity to transfer protection to naive recipients. These studies show that probiotic (VSL#3) administration during a remission period ameliorates the severity of recurrent colitis by inducing an immunoregulatory response involving TGF-β-bearing regulatory cells.
Laurence E Fried - One of the best experts on this subject based on the ideXlab platform.
-
pressure induced phase transition in 1 3 5 triamino 2 4 6 Trinitrobenzene tatb
Applied Physics Letters, 2019Co-Authors: Brad A Steele, Laurence E Fried, Samantha M Clarke, Matthew P Kroonblawd, Ifeng W Kuo, Philip F Pagoria, Sergey Tkachev, Jesse S Smith, Sorin Bastea, Joseph M ZaugAbstract:Determining the unreacted equation of state of 1,3,5-triamino-2,4,6-Trinitrobenzene (TATB) is challenging because it exhibits low crystal symmetry and low X-ray scattering strength. Here, we present the first high-pressure single-crystal X-ray diffraction (SXD) study of this material. Our SXD results reveal a previously unknown transition to a monoclinic phase above 4 GPa. No abrupt change of the volume occurs but the compressibility changes. Concomitant first principles evolutionary crystal structure prediction USPEX calculations confirm this transition and show that it involves a pressure-induced in-plane shift of the layers of TATB molecules with respect to the ambient-pressure phase.
-
the solubility and recrystallization of 1 3 5 triamino 2 4 6 Trinitrobenzene in a 3 ethyl 1 methylimidazolium acetate dmso co solvent system
New Journal of Chemistry, 2009Co-Authors: Yongjin T Han, Philip F Pagoria, Alexander E Gash, Amitesh Maiti, Christine A Orme, Alexander R Mitchell, Laurence E FriedAbstract:Ionic liquids have previously been shown to dissolve strong inter- and intramolecular hydrogen-bonded solids, including natural fibers. Much of this solubility is attributed to the anions in ionic liquids, which can disrupt hydrogen bonding. We have studied the solubility and recrystallization of 1,3,5-triamino-2,4,6-Trinitrobenzene (TATB), a very strong inter- and intramolecular hydrogen-bonded solid, in various ionic liquid solvent systems. We discovered that acetate-based ionic liquids were the best solvents for dissolving TATB, while other anions, such as Cl−, HSO4− and NO3− showed moderate improvements in the solubility compared to conventional organic solvents. Ionic liquid–DMSO co-solvent systems were also investigated for dissolving and recrystallizing TATB.
-
electronic structure of solid 1 3 5 triamino 2 4 6 Trinitrobenzene under uniaxial compression possible role of pressure induced metallization in energetic materials
Physical Review B, 2003Co-Authors: L H Yang, Laurence E Fried, Jason Quenneville, Todd J MartinezAbstract:The electronic structure of the energetic crystalline solid TATB (1,3,5-triamino-2,4,6-Trinitrobenzene) has been studied as a function of uniaxial compression, in order to examine the insulator-to-metal transition. Both ab initio density-functional theory and configuration interaction methods have been used to determine band gaps. Band-gap closure is found to begin near 47% uniaxial strain. A lower bound for the metallization pressure is predicted at 120 GPa, far above the detonation pressure of TATB. Therefore, we conclude that electronic excitation is not involved in the initial stages of detonation for defect-free crystalline TATB.
Jian Xia - One of the best experts on this subject based on the ideXlab platform.
-
curcumin inhibits Trinitrobenzene sulphonic acid induced colitis in rats by activation of peroxisome proliferator activated receptor gamma
International Immunopharmacology, 2006Co-Authors: Ming Zhang, Changsheng Deng, Jian Xia, Jiaju Zheng, Dan ShengAbstract:Abstract Curcumin is a widely used spice with anti-inflammatory and anti-cancer properties. It has been reported that curcumin held therapeutic effects on experimental colitis by inhibition of nuclear factor kappa B (NF-κB). The peroxisome proliferator-activated receptor gamma (PPARγ) is a nuclear receptor with anti-tumor and anti-inflammatory effects and its activation may inhibit the nuclear translocation of NF-κB. Several studies have shown that PPARγ ligands had an important therapeutic effect in colitis. However there is no report about the alteration of PPARγ in Trinitrobenzene sulphonic acid (TNBS)-induced colitis treated with curcumin. In this study, we administered curcumin (30 mg/kg/day) by intraperitoneal injection immediately after colitis was induced and the injection lasted for two weeks. have evaluated the effects of curcumin on the colitis induced by Trinitrobenzene sulphonic acid (TNBS). Curcumin (30 mg/kg d) was administered by intraperitoneal just after colitis was induced and lasted for two weeks. Therapeutic effects of dexamethasone (Dex, 2 mg/kg d) alone and the combined effects of curcumin + Dex were also examined. We found that curcumin improved long-term survival rate of disease-bearing rats, promoted rat body weight recovery, and decreased macroscopic scores of the colitis. The expression levels of PPARγ, 15-deoxy-D12,14-prostaglandin J 2 (15d-PGJ 2 ) and prostaglandin E 2 (PGE 2 ) were all increased, but the expression level of cyclooxygenase-2 (COX-2) was decreased in rats after administration of curcumin. Treatment with Dex improved PPARγ expression and inhibited the expression of COX-2, 15d-PGJ 2 and PGE 2 . Combined effects of curcumin + Dex were similar to that of Dex. In summary, curcumin showed therapeutic effects on TNBS-induced colitis and the mechanisms by which curcumin exerts its effects may involve activation of PPARγ and its ligands.
-
Curcumin-attenuated Trinitrobenzene sulphonic acid induces chronic colitis by inhibiting expression of cyclooxygenase-2.
World Journal of Gastroenterology, 2006Co-Authors: Hua Jiang, Ming Zhang, Changsheng Deng, Jian XiaAbstract:Curcumin-attenuated Trinitrobenzene sulphonic acid induces chronic colitis by inhibiting expression of cyclooxygenase-2
Ming Zhang - One of the best experts on this subject based on the ideXlab platform.
-
curcumin inhibits Trinitrobenzene sulphonic acid induced colitis in rats by activation of peroxisome proliferator activated receptor gamma
International Immunopharmacology, 2006Co-Authors: Ming Zhang, Changsheng Deng, Jian Xia, Jiaju Zheng, Dan ShengAbstract:Abstract Curcumin is a widely used spice with anti-inflammatory and anti-cancer properties. It has been reported that curcumin held therapeutic effects on experimental colitis by inhibition of nuclear factor kappa B (NF-κB). The peroxisome proliferator-activated receptor gamma (PPARγ) is a nuclear receptor with anti-tumor and anti-inflammatory effects and its activation may inhibit the nuclear translocation of NF-κB. Several studies have shown that PPARγ ligands had an important therapeutic effect in colitis. However there is no report about the alteration of PPARγ in Trinitrobenzene sulphonic acid (TNBS)-induced colitis treated with curcumin. In this study, we administered curcumin (30 mg/kg/day) by intraperitoneal injection immediately after colitis was induced and the injection lasted for two weeks. have evaluated the effects of curcumin on the colitis induced by Trinitrobenzene sulphonic acid (TNBS). Curcumin (30 mg/kg d) was administered by intraperitoneal just after colitis was induced and lasted for two weeks. Therapeutic effects of dexamethasone (Dex, 2 mg/kg d) alone and the combined effects of curcumin + Dex were also examined. We found that curcumin improved long-term survival rate of disease-bearing rats, promoted rat body weight recovery, and decreased macroscopic scores of the colitis. The expression levels of PPARγ, 15-deoxy-D12,14-prostaglandin J 2 (15d-PGJ 2 ) and prostaglandin E 2 (PGE 2 ) were all increased, but the expression level of cyclooxygenase-2 (COX-2) was decreased in rats after administration of curcumin. Treatment with Dex improved PPARγ expression and inhibited the expression of COX-2, 15d-PGJ 2 and PGE 2 . Combined effects of curcumin + Dex were similar to that of Dex. In summary, curcumin showed therapeutic effects on TNBS-induced colitis and the mechanisms by which curcumin exerts its effects may involve activation of PPARγ and its ligands.
-
Curcumin-attenuated Trinitrobenzene sulphonic acid induces chronic colitis by inhibiting expression of cyclooxygenase-2.
World Journal of Gastroenterology, 2006Co-Authors: Hua Jiang, Ming Zhang, Changsheng Deng, Jian XiaAbstract:Curcumin-attenuated Trinitrobenzene sulphonic acid induces chronic colitis by inhibiting expression of cyclooxygenase-2
