Publications
1032 results found
Caramori G, Adcock I, 2003, Pharmacology of airway inflammation in asthma and COPD, PULMONARY PHARMACOLOGY & THERAPEUTICS, Vol: 16, Pages: 247-277, ISSN: 1094-5539
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- Citations: 72
Adcock IM, Maneechotesuwan K, Usmani O, 2002, Molecular interactions between glucocorticoids and long-acting β<inf>2</inf>-agonists, Journal of Allergy and Clinical Immunology, Vol: 110, ISSN: 0091-6749
β2-Adrenergic receptor agonists and glucocorticoids are the two most effective treatments for asthma, and used in combination they are more effective than either alone. Glucocorticoids mediate their anti-inflammatory effects through the action of activated glucocorticoid receptors (GRs), with the level of activity being related to the number of nuclear receptors. Glucocorticoids can upregulate the synthesis of several genes in human lung cells through interaction with specific DNA binding regions (glucocorticoid response elements) within the promoter region of glucocorticoid-responsive genes. Many of the down-regulating effects of GRs on the synthesis of cytokines and other inflammatory mediators are due to repression of other transcription factors, such as activator protein-1 and nuclear factor κB. GR functions such as nuclear localization and gene activation can be regulated by phosphorylation status. Long-acting β2-agonists may affect GR nuclear localization through modulation of GR phosphorylation and furthermore through priming of GR functions within the nucleus by modifying GR or GR-associated protein phosphorylation. Glucocorticoids in turn may regulate β2-adrenergic receptor function by increasing its expression, acting through glucocorticoid response elements, and, importantly, by restoring G-protein-β2-receptor coupling and inhibiting β2-receptor down-regulation, thereby preventing desensitization.
Usmani OS, Maneechotesuwan K, Adcock IM, et al., 2002, Glucocorticoid receptor activation in induced sputum following inhaled long-acting β2-agonist and glucocorticoid treatment, Winter Meeting of the British-Thoracic-Society, Publisher: BRITISH MED JOURNAL PUBL GROUP, ISSN: 0040-6376
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- Citations: 1
Yanagawao H, Adcock IM, Hewitt AL, et al., 2002, Effects of long acting β agonists and steroids on cytokine expression, Winter Meeting of the British-Thoracic-Society, Publisher: BRITISH MED JOURNAL PUBL GROUP, ISSN: 0040-6376
Adcock IM, Maneechotesuwan K, Usmani O, 2002, Molecular interactions between glucocorticoids and long-acting beta2-agonists., J Allergy Clin Immunol, Vol: 110, Pages: S261-S268, ISSN: 0091-6749
beta(2)-Adrenergic receptor agonists and glucocorticoids are the two most effective treatments for asthma, and used in combination they are more effective than either alone. Glucocorticoids mediate their anti-inflammatory effects through the action of activated glucocorticoid receptors (GRs), with the level of activity being related to the number of nuclear receptors. Glucocorticoids can upregulate the synthesis of several genes in human lung cells through interaction with specific DNA binding regions (glucocorticoid response elements) within the promoter region of glucocorticoid-responsive genes. Many of the down-regulating effects of GRs on the synthesis of cytokines and other inflammatory mediators are due to repression of other transcription factors, such as activator protein-1 and nuclear factor kappaB. GR functions such as nuclear localization and gene activation can be regulated by phosphorylation status. Long-acting beta(2)-agonists may affect GR nuclear localization through modulation of GR phosphorylation and furthermore through priming of GR functions within the nucleus by modifying GR or GR-associated protein phosphorylation. Glucocorticoids in turn may regulate beta(2)-adrenergic receptor function by increasing its expression, acting through glucocorticoid response elements, and, importantly, by restoring G-protein-beta(2)-receptor coupling and inhibiting beta(2)-receptor downregulation, thereby preventing desensitization.
Eynott PR, Groneberg DA, Caramori G, et al., 2002, Role of nitric oxide in allergic inflammation and bronchial hyperresponsiveness (vol 452, pg 123, 2002), EUROPEAN JOURNAL OF PHARMACOLOGY, Vol: 455, Pages: 79-79, ISSN: 0014-2999
Fujii Y, Tomita K, Sano H, et al., 2002, Dissociation of DNA damage and mitochondrial injury caused by hydrogen peroxide in SV-40 transformed lung epithelial cells, Cancer Cell International, Vol: 2, ISSN: 1475-2867
Adcock I, 2002, Novel targets in inflammation research, Pages: 479-482, ISSN: 1023-3830
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- Citations: 1
Adcock I, 2002, Novel targets in inflammation research. Report from the joint BIRAs/GREMI meeting at Nottingham University UK on 11th-12th April 2002. British Inflammation Research Association. Groupe de Recherche et d'Etude des Mediateurs de l'Inflammation., Inflamm Res, Vol: 51, Pages: 479-482, ISSN: 1023-3830
Eynott PR, Groneberg DA, Caramori G, et al., 2002, Role of nitric oxide in allergic inflammation and bronchial hyperresponsiveness, EUROPEAN JOURNAL OF PHARMACOLOGY, Vol: 452, Pages: 123-133, ISSN: 0014-2999
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- Citations: 61
Tomita K, Caramori G, Lim S, et al., 2002, Increased p21<SUP>CIP1/WAF1</SUP> and B cell lymphoma leukemia-x<sub>L</sub> expression and reduced apoptosis in alveolar macrophages from smokers, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 166, Pages: 724-731, ISSN: 1073-449X
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- Citations: 100
Di Stefano A, Caramori G, Oates T, et al., 2002, Increased expression of nuclear factor-κB in bronchial biopsies from smokers and patients with COPD, EUROPEAN RESPIRATORY JOURNAL, Vol: 20, Pages: 556-563, ISSN: 0903-1936
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- Citations: 315
Zhang XZ, Moilanen E, Adcock IM, et al., 2002, Divergent effect of mometasone on human eosinophil and neutrophil apoptosis, LIFE SCIENCES, Vol: 71, Pages: 1523-1534, ISSN: 0024-3205
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- Citations: 55
Bolger AP, Sharma R, von Haehling S, et al., 2002, Effect of interleukin-10 on the production of tumor necrosis factor-alpha by peripheral blood mononuclear cells from patients with chronic heart failure, AMERICAN JOURNAL OF CARDIOLOGY, Vol: 90, Pages: 384-389, ISSN: 0002-9149
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- Citations: 73
Ito K, Caramori G, Lim S, et al., 2002, Expression and activity of histone deacetylases in human asthmatic airways, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 166, Pages: 392-396, ISSN: 1073-449X
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- Citations: 244
Adcock I, 2002, Role of mediators in late-phase allergic symptoms including congestion, Clinical and Experimental Allergy Reviews, Vol: 2, Pages: 85-88, ISSN: 1472-9725
Chronic nasal congestion is a common symptom of persistent allergic rhinitis and is less easy to resolve than the neurally mediated symptoms of nasal itch and sneeze. It is considered to be a result of inflammatory processes, in particular the persistent inflammatory response linked to the late phase after allergen exposure. Current understanding of the involvement of the various late-phase mediators in the development of nasal congestion is derived from the measurement of inflammatory mediators in nasal lavage fluid of allergic rhinitis sufferers, nasal biopsy and nasal challenge studies. Studies of this type have highlighted the importance of the various late-phase inflammatory mediators, including histamine. This review focuses on the complex late-response inflammatory processes thought to underlie the pathogenesis of chronic nasal congestion, and discusses the recent evidence for the action of some antihistamines at various stages of the late-phase allergic cascade. © 2002 Blackwell Publishing Ltd.
Ito K, Lim S, Caramori G, et al., 2002, A molecular mechanism of action of theophylline: Induction of histone deacetylase activity to decrease inflammatory gene expression, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 99, Pages: 8921-8926, ISSN: 0027-8424
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- Citations: 377
Irusen E, Matthews JG, Takahashi A, et al., 2002, p38 mitogen-activated protein kinase-induced glucocorticoid receptor phosphorylation reduces its activity: Role in steroid-insensitive asthma, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 109, Pages: 649-657, ISSN: 0091-6749
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- Citations: 329
Ravenna F, Caramori G, Panella GL, et al., 2002, An unusual case of congenital short trachea with very long bronchi mimicking bronchial asthma, THORAX, Vol: 57, Pages: 372-373, ISSN: 0040-6376
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- Citations: 7
Tomita K, Lim S, Hanazawa T, et al., 2002, Attenuated production of intracellular IL-10 and IL-12 in monocytes from patients with severe asthma, CLINICAL IMMUNOLOGY, Vol: 102, Pages: 258-266, ISSN: 1521-6616
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- Citations: 43
Ito K, Adcock IM, 2002, Histone acetylation and histone deacetylation, Applied Biochemistry and Biotechnology - Part B Molecular Biotechnology, Vol: 20, Pages: 99-106, ISSN: 1073-6085
Regulation of inflammatory gene transcription is controlled, at least in part, by the degree of local unwinding of nucleosomal DNA. This unwinding is regulated by histone acetylation - increased acetylation results in a more loosely wound structure allowing access of basal transcription factors and RNA polymerase II. In contrast hypoacetylation of histones leads to tighter winding of DNA and reduced gene transcription. In this article we describe methods for measuring the histone acetyltransferase (HAT) and deacetylase (HDAC) activity of A549 cells. We initially describe methods examine whole cell HAT and HDAC activities and subsequently describe a technique for examining HAT activity associated with a specific co-activator CBP isolated by immunoprecipitation. These methods can also be applied to protein extracts from primary cells and from biopsy samples.
Chapman NR, Rocha S, Adcock IM, et al., 2002, Chapter 5 NF-κB function in inflammation, cellular stress and disease, Vol: 3, Pages: 61-73, ISSN: 1568-1254
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- Citations: 5
Ito K, Adcock IM, 2002, Histone acetylation and histone deacetylation, MOLECULAR BIOTECHNOLOGY, Vol: 20, Pages: 99-106, ISSN: 1073-6085
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- Citations: 44
Adcock IM, Chung KF, 2002, Overview: why are corticosteroids ineffective in COPD?, Curr Opin Investig Drugs, Vol: 3, Pages: 58-60, ISSN: 1472-4472
Adcock IM, Ito K, 2002, Molecular mechanisms of steroid actions, Conference of the NATO-Advanced-Study-Institute on Disease Markers in Exhaled Breath, Publisher: IOS PRESS, Pages: 151-158, ISSN: 1566-7693
Chapman NR, Rocha S, Adcock IM, et al., 2002, NF-B function in inflammation, cellular stress and disease, Sensing, signaling and cell adaptation, Pages: 61-73, ISBN: 9780444511478
Barnes PJ, 2002, New treatments for COPD, Clinical management of chronic obstructive pulmonary disease, Pages: 943-963, ISBN: 9780824706104
Tsaprouni LG, Ito K, Punchard N, et al., 2002, Triamcinolone acetonide and dexamethasome suppress TNF-α-induced histone H4 acetylation on lysine residues 8 and 12 in mononuclear cells, CELL SIGNALING, TRANSCRIPTION, AND TRANSLATION AS THERAPEUTIC TARGETS, Vol: 973, Pages: 481-483, ISSN: 0077-8923
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- Citations: 15
Pulleyn LJ, Newton R, Adcock IM, et al., 2001, TGFβ1 allele association with asthma severity, HUMAN GENETICS, Vol: 109, Pages: 623-627, ISSN: 0340-6717
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- Citations: 156
Oliver B, Tomita K, Keller A, et al., 2001, Low-dose theophylline does not exert its anti-inflammatory effects in mild asthma through upregulation of interleukin-10 in alveolar macrophages, ALLERGY, Vol: 56, Pages: 1087-1090, ISSN: 0105-4538
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- Citations: 14
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