The Experts below are selected from a list of 162 Experts worldwide ranked by ideXlab platform
Maria G Belvisi - One of the best experts on this subject based on the ideXlab platform.
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critical role for t cells in Sephadex induced airway inflammation pharmacological and immunological characterization and molecular biomarker identification
Journal of Immunology, 2002Co-Authors: Elbdaoui Haddad, Stephen Underwood, Dominika Dabrowski, Mark A Birrell, Kerryn Mccluskie, Cliff H Battram, Michaela Pecoraro, Martyn Foster, Maria G BelvisiAbstract:Intratracheal instillation of Sephadex particles is a convenient model for assessing the impact of potential anti-inflammatory compounds on lung eosinophilia thought to be a key feature in asthma pathophysiology. However, the underlying cellular and molecular mechanisms involved are poorly understood. We have studied the time course of Sephadex-induced lung eosinophilia, changes in pulmonary T cell numbers, and gene and protein expression as well as the immunological and pharmacological modulation of these inflammatory indices in the Sprague Dawley rat. Sephadex increased T cell numbers (including CD4+ T cells) and evoked a pulmonary eosinophilia that was associated with an increase in gene/protein expression of the Th2-type cytokines IL-4, IL-5, and IL-13 and eotaxin in lung tissue. Sephadex instillation also induced airway hyperreactivity to acetylcholine and bradykinin. A neutralizing Ab (R73) against the αβ-TCR caused 54% depletion of total (CD2+) pulmonary T cells accompanied by a significant inhibition of IL-4, IL-13 and eotaxin gene expression together with suppression (65% inhibition) of eosinophils in lung tissue 24 h after Sephadex treatment. Sephadex-induced eosinophilia and Th2 cytokine gene and/or protein expression were sensitive to cyclosporin A and budesonide, compounds that inhibit T cell function, suggesting a pivotal role for T cells in orchestrating Sephadex-induced inflammation in this model.
David R Engelke - One of the best experts on this subject based on the ideXlab platform.
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Sephadex binding rna ligands rapid affinity purification of rna from complex rna mixtures
Nucleic Acids Research, 2001Co-Authors: Chatchawan Srisawat, Irwin J Goldstein, David R EngelkeAbstract:Sephadex-binding RNA ligands (aptamers) were obtained through in vitro selection. They could be classified into two groups based on their consensus sequences and the aptamers from both groups showed strong binding to Sephadex G-100. One of the highest affinity aptamers, D8, was chosen for further characterization. Aptamer D8 bound to dextran B512, the soluble base material of Sephadex, but not to isomaltose, isomaltotriose and isomaltotetraose, suggesting that its optimal binding site might consist of more than four glucose residues linked via α-1,6 linkages. The aptamer was very specific to the Sephadex matrix and did not bind appreciably to other supporting matrices, such as Sepharose, Sephacryl, cellulose or pustulan. Using Sephadex G-100, the aptamer could be purified from a complex mixture of cellular RNA, giving an enrichment of at least 60 000-fold, compared with a non-specific control RNA. These RNA aptamers can be used as affinity tags for RNAs or RNA subunits of ribonucleoproteins to allow rapid purification from complex mixtures of RNA using only Sephadex.
Elbdaoui Haddad - One of the best experts on this subject based on the ideXlab platform.
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critical role for t cells in Sephadex induced airway inflammation pharmacological and immunological characterization and molecular biomarker identification
Journal of Immunology, 2002Co-Authors: Elbdaoui Haddad, Stephen Underwood, Dominika Dabrowski, Mark A Birrell, Kerryn Mccluskie, Cliff H Battram, Michaela Pecoraro, Martyn Foster, Maria G BelvisiAbstract:Intratracheal instillation of Sephadex particles is a convenient model for assessing the impact of potential anti-inflammatory compounds on lung eosinophilia thought to be a key feature in asthma pathophysiology. However, the underlying cellular and molecular mechanisms involved are poorly understood. We have studied the time course of Sephadex-induced lung eosinophilia, changes in pulmonary T cell numbers, and gene and protein expression as well as the immunological and pharmacological modulation of these inflammatory indices in the Sprague Dawley rat. Sephadex increased T cell numbers (including CD4+ T cells) and evoked a pulmonary eosinophilia that was associated with an increase in gene/protein expression of the Th2-type cytokines IL-4, IL-5, and IL-13 and eotaxin in lung tissue. Sephadex instillation also induced airway hyperreactivity to acetylcholine and bradykinin. A neutralizing Ab (R73) against the αβ-TCR caused 54% depletion of total (CD2+) pulmonary T cells accompanied by a significant inhibition of IL-4, IL-13 and eotaxin gene expression together with suppression (65% inhibition) of eosinophils in lung tissue 24 h after Sephadex treatment. Sephadex-induced eosinophilia and Th2 cytokine gene and/or protein expression were sensitive to cyclosporin A and budesonide, compounds that inhibit T cell function, suggesting a pivotal role for T cells in orchestrating Sephadex-induced inflammation in this model.
Naihong Chen - One of the best experts on this subject based on the ideXlab platform.
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anti inflammatory effect of immlg5521 a coumarin derivative on Sephadex induced lung inflammation in rats
International Immunopharmacology, 2012Co-Authors: Zhipeng Li, Jinfeng Hu, Haijie Ji, Naihong ChenAbstract:Abstract The study is to investigate the effect of compound IMMLG5521, a coumarin derivative, on lung inflammation induced by Sephadex in rats. Sephadex led to massive granulomas, infiltration of neutrophils and eosinophils, the increase of TNF-α level in BALF and lung tissue. Sephadex injection led to the up-regulation of VCAM-1 and ICAM-1 expressions in the lungs. However, pretreatment with IMMLG5521 (6.25 and 12.5 mg/kg) inhibited massive granulomas and infiltration of neutrophils and eosinophils, decreased TNF-α level in BALF and lung tissue, and down-regulated VCAM-1 and ICAM-1 expressions in the lung tissue. In conclusion, compound IMMLG5521 may suppress the lung injury induced by Sephadex, at least in part, due to the prevention of the up-regulation of VCAM-1 and ICAM-1 expressions and TNF-α level.
Carlo Alberto Maggi - One of the best experts on this subject based on the ideXlab platform.
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role of tachykinins in Sephadex induced airway hyperreactivity and inflammation in guinea pigs
European Journal of Pharmacology, 2002Co-Authors: Manuela Tramontana, Paolo Santicioli, Sandro Giuliani, Rosemarie Catalioto, Alessandro Lecci, F Carini, Carlo Alberto MaggiAbstract:Abstract We have studied the effect of selective tachykinin NK 1 and NK 2 receptor antagonists on airway hyperreactivity to acetylcholine and increase of inflammatory cells on bronchoalveolar lavage fluid induced by Sephadex beads (20 mg/kg, i.v.) in guinea pigs. Airway hyperreactivity was assessed by measuring the increase of bronchial insufflation pressure to acetylcholine (0.01–30 μmol/kg, i.v.) at 3 h (early phase) and 24 h (late phase) after Sephadex administration. An increase in inflammatory cells in bronchoalveolar lavage fluid (eosinophils and macrophages) was detected at 24 h (from 11.6·10 6 to 49.3·10 6 cells) but not at 3 h from Sephadex administration. Neurokinin A and substance P levels in bronchoalveolar lavage fluid showed a significant increase at 24 h (from 31.7±11.6 to 561±231 pg/ml and from 5.9±2.6 to 29.3±4.1 pg/ml for neurokinin A and substance P, respectively). At this time point, the tachykinin in bronchoalveolar lavage cellular content was depleted from 232±43 to 21±20 pg/sample and from 56.6±6.7 to 2±2 pg/sample for neurokinin A and substance P, respectively. Capsaicin pretreatment abolished the early but not the late phase of airway hyperreactivity induced by Sephadex without modifying bronchoalveolar lavage total cells number and bronchoalveolar lavage levels of neurokinin A and substance P. Administration of the tachykinin NK 2 (nepadutant) and/or the NK 1 receptor antagonist (MEN 11467 or (1 R ,2 S )-2- N [1( H )indol-3-yl-carbonyl]-1- N [ N -( p -tolylacetyl)- N -(methyl)- d -3(2-naphthyl)alanyl}diaminocyclohexane)), 5 min before Sephadex, prevented the early phase of airway hyperreactivity to acetylcholine but only nepadutant prevented the late phase. Nepadutant was able to abolish the early phase of airway hyperreactivity if given after Sephadex administration and reduced by about 50% the increase of cell number in bronchoalveolar lavage fluid during the late phase, without affecting the levels of neurokinin A and substance P. These findings indicate an involvement of endogenous tachykinins in the genesis of airway hyperreactivity in a guinea-pig model of non-allergic asthma. Early airway hyperreactivity apparently involves release of tachykinins from capsaicin-sensitive afferent nerves acting via tachykinin NK 1 /NK 2 receptors. Late airway hyperreactivity involves tachykinins acting via tachykinin NK 2 receptors: inflammatory cells activated/recruited in response to Sephadex challenge appear a likely source of tachykinins involved in the late phase of the response.