Publications
157 results found
Telcian AG, Laza-Stanca V, Edwards MR, et al., 2011, RSV-Induced Bronchial Epithelial Cell PD-L1 Expression Inhibits CD8<SUP>+</SUP> T Cell Nonspecific Antiviral Activity, JOURNAL OF INFECTIOUS DISEASES, Vol: 203, Pages: 85-94, ISSN: 0022-1899
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- Citations: 58
Vareille M, Kieninger E, Edwards MR, et al., 2011, The Airway Epithelium: Soldier in the Fight against Respiratory Viruses, CLINICAL MICROBIOLOGY REVIEWS, Vol: 24, Pages: 210-+, ISSN: 0893-8512
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- Citations: 423
Bartlett NW, Walton RP, Edwards MR, et al., 2011, Type I Interferon Regulates Antiviral And Inflammatory Responses To Rhinovirus Infection In Vivo, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Hewson CA, Haas JJ, Bartlett NW, et al., 2010, Rhinovirus induces MUC5AC in a human infection model and <i>in vitro via</i> NF-κB and EGFR pathways, EUROPEAN RESPIRATORY JOURNAL, Vol: 36, Pages: 1425-1435, ISSN: 0903-1936
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- Citations: 84
Stokes CA, Dick EP, Bennett JA, et al., 2010, THE ROLE OF MYD88 IN RHINOVIRUS 1B INFECTION, British-Thoracic-Society-Winter-Meeting 2010, Publisher: B M J PUBLISHING GROUP, Pages: A37-A38, ISSN: 0040-6376
Slater L, Bartlett NW, Haas JJ, et al., 2010, Co-ordinated Role of TLR3, RIG-I and MDA5 in the Innate Response to Rhinovirus in Bronchial Epithelium, PLOS PATHOGENS, Vol: 6, ISSN: 1553-7366
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- Citations: 238
Gielen V, Johnston SL, Edwards MR, 2010, Azithromycin induces anti-viral responses in bronchial epithelial cells, EUROPEAN RESPIRATORY JOURNAL, Vol: 36, Pages: 646-654, ISSN: 0903-1936
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- Citations: 209
Edwards MR, Bartlett NW, Slater L, et al., 2010, ATS Abstract: IKK-ß Is Required For Rhinovirus Induced IFN-ß, IFN-» And Pro-inflammatory Cytokine Production In Vitro And In Vivo, American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans, Publisher: American Thoracic Society
Johnston SL, Edwards MR, 2009, Mechanisms of adverse effects of β-agonists in asthma, THORAX, Vol: 64, Pages: 739-741, ISSN: 0040-6376
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- Citations: 27
Khaitov MR, Laza-Stanca V, Edwards MR, et al., 2009, Respiratory virus induction of alpha-, beta- and lambda-interferons in bronchial epithelial cells and peripheral blood mononuclear cells, ALLERGY, Vol: 64, Pages: 375-386, ISSN: 0105-4538
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- Citations: 162
Edwards MR, Bartlett NW, Clarke D, et al., 2009, Targeting the NF-κB pathway in asthma and chronic obstructive pulmonary disease, PHARMACOLOGY & THERAPEUTICS, Vol: 121, Pages: 1-13, ISSN: 0163-7258
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- Citations: 305
Slater L, Haas JJ, Edwards MR, et al., 2009, Indentification of Signalling Kinases Required for Rhinovirus Induction of Type I IFN-β & Type III IFN-λ Production in HBECs, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 179, ISSN: 1073-449X
Sykes A, Edwards MR, Haas JJ, et al., 2009, Interferon & RNA Helicases Responses to TLR3 Recognition in HBECs and PBMCs., AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 179, ISSN: 1073-449X
Haas JJ, Slater L, Kotenko S, et al., 2009, Transcriptional Regulation of RV1B Induced IFN-λ1 Production in Primary Bronchial Epithelial Cells., AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 179, ISSN: 1073-449X
Contoli M, Caramori G, Baraldo S, et al., 2009, Interleukin-4 Modulates Rhinovirus Replication and Antiviral Immune Response in Respiratory Epithelial Cells., AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 179, ISSN: 1073-449X
Gielen V, Johnston SL, Edwards MR, 2009, Azithromycin Increases Interferon and Interferon Stimulated Gene Expression and Has Anti-Rhinoviral Activity in Human Bronchial Epithelial Cells, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 179, ISSN: 1073-449X
Edwards MR, Slater L, Bartlett NW, et al., 2009, The Innate Response to Rhinovirus in Bronchial Epithelial Cells Is Controlled by Both TLR3 and RNA Helicase Mediated Signalling Pathways, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 179, ISSN: 1073-449X
Edwards MR, Johnston SL, 2008, Deficient interferon in virus-induced asthma exacerbations, CLINICAL AND EXPERIMENTAL ALLERGY, Vol: 38, Pages: 1416-1418, ISSN: 0954-7894
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- Citations: 9
Papi A, Contoli M, Gasparini P, et al., 2008, Role of xanthine oxidase activation and reduced glutathione depletion in rhinovirus induction of inflammation in respiratory epithelial cells., The Journal of Biological chemistry, Vol: 283, Pages: 28595-28606
Bartlett NW, Walton RP, Edwards MR, et al., 2008, Mouse models of rhinovirus-induced disease and exacerbation of allergic airway inflammation, NATURE MEDICINE, Vol: 14, Pages: 199-204, ISSN: 1078-8956
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- Citations: 285
Khaitov MR, Laza-Stanca V, Edwards MR, et al., 2008, Type I and type III interferon expression during rhinovirus infection, 64th Annual Meeting of the American-Academy-of-Allergy-Asthma-and-Immunology, Publisher: MOSBY-ELSEVIER, Pages: S119-S119, ISSN: 0091-6749
Edwards MR, Slater L, Johnston SL, 2007, Signalling pathways mediating type I interferon gene expression, MICROBES AND INFECTION, Vol: 9, Pages: 1245-1251, ISSN: 1286-4579
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- Citations: 19
Edwards MR, Haas J, Panettieri RA, et al., 2007, Corticosteroids and beta(2) Agonists differentially regulate rhinovirus-induced interleukin-6 via distinct cis-acting elements, Journal of Biological Chemistry, Vol: 282, Pages: 15366-15375, ISSN: 1083-351X
Interleukin-6 (IL-6) is a proinflammatory cytokine up-regulated by rhinovirus infection during acute exacerbations of asthma and chronic obstructive pulmonary disease. The role of IL-6 during exacerbations is unclear; however, it is believed IL-6 could contribute to airway and systemic inflammation. In this study we investigate the effects of common asthma treatments fluticasone propionate and β2 agonists salmeterol and salbutamol on IL-6 production in BEAS-2B and primary bronchial epithelial cells. Salmeterol and salbutamol enhanced rhinovirus- and IL-1β-induced IL-6 production; however, fluticasone treatment caused a reduction of IL-6 protein and mRNA. Combined activity of salmeterol and fluticasone at equimolar concentrations had no effect on rhinovirus or IL-1β induction of IL-6. The induction of IL-6 by salmeterol was dependent upon the β2 receptor and could also be induced by cAMP or cAMP-elevating agents forskolin and rolipram. Using transfection of IL-6 promoter reporter constructs, dominant negative mutants, and electromobility shift assays, it was found that NF-κB was the only transcription factor required for rhinovirus induction of IL-6 gene expression. Salmeterol caused an augmentation of rhinovirus-induced promoter activation via a mechanism dependent upon the c/EBP and/or CRE (cyclic AMP response element) cis-acting sites. The suppressive effect of FP was dependent upon distinct glucocorticoid response element sequences proximal to the transcriptional start site within the IL-6 promoter. The data demonstrate that β2 agonists can augment IL-6 expression by other stimuli in an additive manner via cyclic AMP and that the negative effect of steroids is mediated by glucocorticoid response elements within the IL-6 promoter.
Edwards MR, Hewson CA, Laza-Stanca V, et al., 2007, Protein kinase R, IκB kinase-β and NF-κB are required for human rhinovirus induced pro-inflammatory cytokine production in bronchial epithelial cells, MOLECULAR IMMUNOLOGY, Vol: 44, Pages: 1587-1597, ISSN: 0161-5890
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- Citations: 32
Khuu CH, Barrozo RM, Hai T, et al., 2007, Activating transcription factor 3 (ATF3) represses the expression of CCL4 in murine macrophages., Mol Immunol, Vol: 44, Pages: 1598-1605, ISSN: 0161-5890
Acute expression of macrophage inflammatory protein-1 beta (also known as CCL4) promotes beneficial leukocyte recruitment to infected tissues, but chronic expression of this chemokine contributes to inflammatory disease. CCL4 expression is controlled largely at the transcriptional level and an ATF/CRE sequence located in the promoter (-104 to -97bp, relative to the transcriptional start site) has been identified as a critical cis-acting element. The trans-acting binding proteins that influence CCL4 transcription via this site are largely unknown. We investigated whether activating transcription factor 3 (ATF3), a member of the ATF/CREB family of transcription factors, binds to the CCL4 ATF/CRE site in macrophages. Using the electrophoretic mobility shift assay and the chromatin immunoprecipitation assay, we found that ATF3 binds to the ATF/CRE site within the CCL4 promoter in untreated and lipopolysaccharide (LPS)-stimulated macrophages. Quantitative RT-PCR analysis showed that CCL4 mRNA levels in elicited peritoneal macrophages from ATF3(-/-) mice are significantly higher than in congenic ATF3(+/+) macrophages under both unstimulated and LPS-stimulated conditions, suggesting that ATF3 represses transcription of the CCL4 gene. Consistent with the higher gene expression, ATF3-deficient macrophages secreted more CCL4 protein than ATF3(+/+) macrophages. Similar results were obtained in bone-marrow-derived macrophages treated with Toll-like receptor 2, 3, 4 and 5 agonists. Thus, we conclude that ATF3 constitutively binds to the ATF/CRE site in the CCL4 promoter where it represses basal and pathogen-associated molecular pattern (PAMP)-stimulated transcription. Consequently, ATF3 appears to be part of a control mechanism that limits the amount of CCL4 released by macrophages, preventing excessive inflammation.
Contoli M, Message SD, Laza-Stanca V, et al., 2006, Role of deficient type III interferon-λ production in asthma exacerbations, NATURE MEDICINE, Vol: 12, Pages: 1023-1026, ISSN: 1078-8956
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- Citations: 799
Laza-Stanca V, Stanciu LA, Message SD, et al., 2006, Rhinovirus replication in human macrophages induces NF-κB-dependent tumor necrosis factor alpha production, JOURNAL OF VIROLOGY, Vol: 80, Pages: 8248-8258, ISSN: 0022-538X
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- Citations: 84
Edwards MR, Johnson MW, Johnston SL, 2006, Combination therapy - Synergistic suppression of virus-induced chemokines in airway epithelial cells, AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, Vol: 34, Pages: 616-624, ISSN: 1044-1549
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- Citations: 85
Khaitov MR, Laza-Stantca V, Edwards MR, et al., 2006, [Production of alpha-, beta-, and lambda-interferons by epithelial and mononuclear cells during acute respiratory viral infection]., Zh Mikrobiol Epidemiol Immunobiol, Pages: 63-69, ISSN: 0372-9311
Role of several types of cells (human broncho-epithelial cells, BEAS-2B cell line, and mononuclear cells as model of macrophages) in production of alpha-, beta- and lambda-interferons during acute respiratory viral infection was studied. Kits for detection of these interferons by quantitative PCR assay has been developed. In human broncho-epithelial cells respiratory viruses induced statistically significant expression of alpha-interferon mRNA at 8 hours after infection, beta-interferon mRNA--at 24 hours after infection, IL-29 mRNA (lambda-interferon) - at 24 hours after infection, IL-28 mRNA (lambda-interferon) - at 8 and 24 hours after infection. In BEAS-2B cell line induction of alpha-interferon mRNA expression was observed at 8 hours after infection, beta-interferon mRNA expression - at 24 hours after infection, IL-29 mRNA (lambda-interferon) expression - at 8 and 24 hours after viral challenge. Production of beta- and lambda-interferons by ELISA at 24 hours after infection has been detected. When polymorphonuclear cells were challenged, induction of alpha-, beta-, and lambda-interferons expression was observed at 8 hours after infection. Production of alpha-, beta- and lambda-interferons has been detected by ELISA at 24 hours after infection by rhinovirus 16.
Edwards MR, Kebadze T, Johnson MW, et al., 2006, New treatment regimes for virus-induced exacerbations of asthma, PULMONARY PHARMACOLOGY & THERAPEUTICS, Vol: 19, Pages: 320-334, ISSN: 1094-5539
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- Citations: 23
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