Publications
753 results found
Bisgaard H, Zielen S, Garcia-Garcia ML, et al., 2005, Montelukast reduces asthma exacerbations in 2-to 5-year-old children with intermittent asthma, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 171, Pages: 315-322, ISSN: 1073-449X
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- Citations: 243
Cho SH, Stanciu LA, Holgate ST, et al., 2005, Increased interleukin-4, interleukin-5, and interferon-γ in airway CD4<SUP>+</SUP> and CD8<SUP>+</SUP> T cells in atopic asthma, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 171, Pages: 224-230, ISSN: 1073-449X
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- Citations: 179
Biscione GL, Corne J, Chauhan AJ, et al., 2005, <i>Chlamydophila pneumoniae</i> in asthma -: From the authors, EUROPEAN RESPIRATORY JOURNAL, Vol: 25, Pages: 392-394, ISSN: 0903-1936
Johnston NW, Johnston SL, Duncan JM, et al., 2005, The September epidemic of asthma exacerbations in children: A search for etiology, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 115, Pages: 132-138, ISSN: 0091-6749
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- Citations: 254
Johnston SL, 2005, Overview of virus-induced airway disease., Proc Am Thorac Soc, Vol: 2, Pages: 150-156, ISSN: 1546-3222
Acute exacerbations of asthma and chronic obstructive pulmonary disease (COPD) are the major cause of morbidity, mortality, and health costs of both diseases. Currently available treatments are poorly effective in both acute treatment of and prevention of acute exacerbations. New treatments for intervention and prophylaxis are therefore required; to facilitate their development, we must understand the causes and mechanisms of exacerbations. Respiratory viral infections (2/3 rhinoviruses) precipitate 80% or more of asthma exacerbations in children, and the majority of exacerbations of asthma and COPD in adults, but mechanisms of virus-induced lower airway inflammation and of host resistance against respiratory viruses are poorly understood. Development of in vitro experimental models of virus infection has identified interferon-beta and nitric oxide as possible therapeutic targets to augment antiviral immunity, and nuclear factor-kappaB as a target for development of anti-inflammatory therapies. In vivo models could also serve to identify and validate targets and as an experimental system to test candidate molecules as they emerge into clinical studies. Studies in asthma have paved the way for development of an asthma model; a similar experimental model in COPD would accelerate development of new therapies for these common diseases with enormous burdens of illness.
Edwards MR, Mukaida N, Johnson M, et al., 2005, IL-1β induces IL-8 in bronchial cells via NF-κB and NF-IL6 transcription factors and can be suppressed by glucocorticoids, PULMONARY PHARMACOLOGY & THERAPEUTICS, Vol: 18, Pages: 337-345, ISSN: 1094-5539
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- Citations: 32
Mallia P, Johnston SL, 2005, Mechanisms and experimental models of chronic obstructive pulmonary disease exacerbations., Proc Am Thorac Soc, Vol: 2, Pages: 361-366, ISSN: 1546-3222
Exacerbations of chronic obstructive pulmonary disease (COPD) are a major cause of morbidity, mortality, and rising health care costs. In addition, they are associated with an accelerated loss of lung function and thus have a direct effect on disease progression. There are few studies examining the cellular and molecular mechanisms of COPD exacerbations. Exacerbations are linked to increased airway inflammation and oxidative stress, but many questions remain unanswered regarding the key inflammatory cells and mediators. Current therapies for COPD exacerbations are of limited effectiveness, and a better understanding of the inflammatory events at exacerbation is required to devise new therapeutic agents. The development of experimental models of exacerbation-for example, the use of experimental rhinovirus infection in humans with COPD-would greatly facilitate studies of exacerbations.
Chauhan AJ, Chatterjee A, Johnston SL, 2005, Acute respiratory infections. In: “Effects of air pollution on children´s health and development”. Krzyzanowski M et al. (eds). 2005 pp 44-69.
Wedzicha JA, Johnston SL, Mitchell DM, 2004, Thorax annual report: 1 October 2003 to 30 September 2004, THORAX, Vol: 59, Pages: 1012-1014, ISSN: 0040-6376
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- Citations: 3
Work PAB, Bucchieri F, Hamilton LM, et al., 2004, Inflammatory mediators release from asthmatic and non-asthmatic bronchial epithelial cells following infection with rhinovirus, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: 17-17, ISSN: 0040-6376
Hoggard N, Rayner DV, Johnston SL, et al., 2004, Peripherally administered [Nle<SUP>4</SUP>,D-Phe<SUP>7</SUP>]-α-melanocyte stimulating hormone increases resting metabolic rate, while peripheral agouti-related protein has no effect, in wild type C57BL/6 and <i>ob/ob</i> mice, JOURNAL OF MOLECULAR ENDOCRINOLOGY, Vol: 33, Pages: 693-703, ISSN: 0952-5041
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- Citations: 35
Wark PAB, Johnston SL, Bucchieri F, et al., 2004, Asthmatic bronchial epithelial cells have deficient innate immune response to infection with rhinovirus, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: 16-17, ISSN: 0040-6376
Hewson CA, Edbrooke MR, Johnston SL, 2004, PMA induces the MUC5AC respiratory mucin in human bronchial epithelial cells, <i>via</i> PKC, EGF/TGF-α, Ras/Raf, MEK, ERK and Sp1-dependent mechanisms, JOURNAL OF MOLECULAR BIOLOGY, Vol: 344, Pages: 683-695, ISSN: 0022-2836
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- Citations: 141
Biscione GL, Corne J, Chauhan AJ, et al., 2004, Increased frequency of detection of <i>Chiamydophila pneumoniae</i> in asthma, EUROPEAN RESPIRATORY JOURNAL, Vol: 24, Pages: 745-749, ISSN: 0903-1936
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- Citations: 41
Wedzicha JA, Johnston SL, Mitchell DM, 2004, Journal impact factors for 2003:: <i>Thorax</i> increases, THORAX, Vol: 59, Pages: 736-736, ISSN: 0040-6376
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- Citations: 5
Papadopoulos NG, Papi A, Psarras S, et al., 2004, Mechanisms of rhinovirus-induced asthma., Paediatr Respir Rev, Vol: 5, Pages: 255-260, ISSN: 1526-0542
Several epidemiological studies using sensitive detection methodologies have confirmed that the majority of acute asthma exacerbations follow upper respiratory tract infections--common colds. Most of these colds are due to human rhinoviruses (RVs). RVs are able to reach and replicate in epithelial cells of the lower airways and can activate these cells to produce pro-inflammatory mediators. Under some circumstances, RVs can also become cytotoxic to the epithelium. Atopic asthmatic individuals produce less interferon-gamma and more interleukin-10 than normal subjects in response to RV infection. Symptom severity as well as viral shedding after experimental RV infection, is inversely correlated with 'atopic' status, expressed as the interferon-gamma to interleukin-5 ratio. Expression of co-stimulatory molecules on immune cells is also affected in atopic asthmatics, suggesting an aberrant immune response to RV that may lead to suboptimal viral clearance and viral persistence. Some of the above effects can be reversed in vitro by corticosteroids, second-generation antihistamines or anti-oxidants; however, the optimal strategy for treating acute asthma exacerbations requires further research at both mechanistic and clinical levels.
Schwarze J, Johnston SL, 2004, Unravelling synergistic immune interactions between respiratory virus infections and allergic airway inflammation, CLINICAL AND EXPERIMENTAL ALLERGY, Vol: 34, Pages: 1153-1155, ISSN: 0954-7894
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- Citations: 4
Myatt TA, Johnston SL, Zuo ZF, et al., 2004, Detection of airborne rhinovirus and its relation to outdoor air supply in office environments, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 169, Pages: 1187-1190, ISSN: 1073-449X
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- Citations: 117
Ison MG, Johnston SL, Openshaw P, et al., 2004, Current research on respiratory viral infections: Fifth International Symposium., Antiviral Res, Vol: 62, Pages: 75-110, ISSN: 0166-3542
Legg JP, Hussain IR, Warner JA, et al., 2004, Type 2 cytokines in respiratory syncytial virus bronchiolitis, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 169, Pages: 1168-1168, ISSN: 1073-449X
Dheda K, Hugget JF, Kim LU, et al., 2004, Type 2 cytokines in respiratory syncytial virus bronchiolitis, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 169, Pages: 1167-1168, ISSN: 1073-449X
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- Citations: 4
Johnston SL, Bell LM, Murray SJ, et al., 2004, Individual variations in resting metabolic rate in C57BL/6J mice do not predispose to weight or fat gain over 6 months on diets of varying fat content, 13th European Congress on Obesity, Publisher: NATURE PUBLISHING GROUP, Pages: S17-S17, ISSN: 0307-0565
Johnston SL, Hill SJ, Lock RJ, et al., 2004, Echocardiographic abnormalities in primary antibody deficiency, POSTGRADUATE MEDICAL JOURNAL, Vol: 80, Pages: 214-218, ISSN: 0032-5473
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- Citations: 19
Wark PA, Johnston SL, Holgate ST, et al., 2004, Interferon-Beta for Anti-Virus Therapy for Respiratory Diseases.
Wark PA, Johnston SL, Holgate ST, et al., 2004, Anti-virus therapy for respiratory diseases. UK patent application No. GB 0405634.7, 12 March 2004.
Wedzicha JA, Johnston SL, Mitchell DM, 2004, Thank you to all <i>Thorax</i> reviewers, THORAX, Vol: 59, Pages: 6-7, ISSN: 0040-6376
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- Citations: 3
Message SD, Johnston SL, 2004, Host defense function of the airway epithelium in health and disease: clinical background, JOURNAL OF LEUKOCYTE BIOLOGY, Vol: 75, Pages: 5-17, ISSN: 0741-5400
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- Citations: 120
Psarras S, Papadopoulos NG, Johnston SL, 2004, Parainfluenza viruses, Principles and Practice of Clinical Virology Fifth Edition, Editors: Zuckerman, Banatvala, Griffiths, Pattison, Schoub, UK, Publisher: John Wiley & Son, Pages: 299-321
Kendall G, Shiu KY, Johnston SL, 2004, Complete Medicine and Surgery, Publisher: Blackwell Science
Psarras S, Papadopoulos NG, Johnston SL, 2004, Pathogenesis of respiratory syncytial virus bronchiolitis-related wheezing., Paediatr Respir Rev, Vol: 5 Suppl A, Pages: S179-S184, ISSN: 1526-0542
Respiratory syncytial virus (RSV) is a common cause of virus infection of the human respiratory tract during the first two years of life, with virtually all children experiencing at least one infection within this period. Although this usually leads to mild respiratory illness, some infants develop more severe disease (bronchiolitis, pneumonia, etc.) affecting the lower airways and frequently requiring hospitalisation. There is evidence that bronchiolitis hospitalisations have increased during the last two decades and many of the hospitalised children develop wheezing later in life. The immune response to the virus is probably a major factor in the development or the expression of the pathological phenotype. In particular, a bias towards type-2 cytokine responses seems to be associated with more severe disease, whereas a type-1 response leads to more effective viral clearance and milder illness. Although the virus by itself triggers a type-1 response, a preexisting type-1 deficiency may contribute to the severity of the disease. In that sense, RSV bronchiolitis may serve as a marker, reflecting predisposition of the individual for virus induced wheezing early in life and/or asthma later in life.
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