Publications
753 results found
Oliver BGG, Lim S, Wark P, et al., 2008, Rhinovirus exposure impairs immune responses to bacterial products in human alveolar macrophages, THORAX, Vol: 63, Pages: 519-525, ISSN: 0040-6376
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- Citations: 115
Newcomb DC, Sajjan US, Nagarkar DR, et al., 2008, Human rhinovirus 1B exposure induces phosphatidylinositol 3-kinase-dependent airway inflammation in mice, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 177, Pages: 1111-1121, ISSN: 1073-449X
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- Citations: 99
Ghannad F, Nica D, Fulle MIG, et al., 2008, Absence of αvβ6 integrin is linked to initiation and progression of periodontal disease, AMERICAN JOURNAL OF PATHOLOGY, Vol: 172, Pages: 1271-1286, ISSN: 0002-9440
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- Citations: 53
Fernandes R, Kusel M, Cyr M, et al., 2008, Cord blood hemopoietic progenitor profiles predict acute respiratory symptoms in infancy, PEDIATRIC ALLERGY AND IMMUNOLOGY, Vol: 19, Pages: 239-247, ISSN: 0905-6157
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- Citations: 15
Walton RP, Johnston SL, 2008, Role of respiratory viral infections in the development of atopic conditions, CURRENT OPINION IN ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 8, Pages: 150-153, ISSN: 1528-4050
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- Citations: 17
Bousquet J, Khaltaev N, Cruz AA, et al., 2008, Allergic Rhinitis and its Impact on Asthma (ARIA) 2008 update (in collaboration with the World Health Organization, GA(2)LEN and AllerGen)., Allergy, Vol: 63 Suppl 86, Pages: 8-160
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
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
Edwards M, Slater L, Haas J, et al., 2008, Transcriptional regulation of type I interferon-β and type III interferon-γ in bronchial epithelial cells.: Common role of the transcription factor IRF-3, 27th Congress of the European-Academy-of-Allergology-and-Clinical-Immunology, Publisher: BLACKWELL PUBLISHING, Pages: 115-115, ISSN: 0105-4538
Bartlett NW, Johnston SL, 2008, Rhinoviruses, Encyclopedia of Virology, Editors: Mahy, Regenmortel, Oxford, Publisher: Elsevier, Pages: 467-475
Stanciu L, Telcian A, Zdrenghea M, et al., 2008, The effect of calcitriol on VDR, RANTES and virus gene expression in rhinovirusinfected respiratory bronchial epithelial cells, 27th Congress of the European-Academy-of-Allergology-and-Clinical-Immunology, Publisher: BLACKWELL PUBLISHING, Pages: 625-625, ISSN: 0105-4538
Telcian A, Stanciu L, Johnston S, 2008, Respiratory Syncytial Virus negatively modulates vitamin D action in respiratory epithelial cells, 27th Congress of the European-Academy-of-Allergology-and-Clinical-Immunology, Publisher: BLACKWELL PUBLISHING, Pages: 59-59, ISSN: 0105-4538
Bousquet J, Khaltaev N, Cruz AA, et al., 2008, Allergic rhinitis and its impact on asthma (ARIA) 2008 update (in collaboration with the World Health Organization, GA<SUP>2</SUP>LEN and AllerGen), ALLERGY, Vol: 63, Pages: 8-+, ISSN: 0105-4538
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- Citations: 3361
Bartlett N, Walton R, Slater L, et al., 2008, Activation of NFκB and induction of T-cell recruiting chemokines by rhinovirus infection <i>in vitro</i> and <i>in vivo</i>, 27th Congress of the European-Academy-of-Allergology-and-Clinical-Immunology, Publisher: BLACKWELL PUBLISHING, Pages: 115-115, ISSN: 0105-4538
Mallia P, Johnston SL, 2008, Viral Infections and Chronic Obstructive Pulmonary Disease. In: Chronic Obstructive Lung Diseases 2. Voelkel NF & MacNee W (eds). BC Dekker Inc 2008 pp 205-218.
Footitt J, Sykes A, Mallia P, et al., 2008, Comparison of Asthma and COPD Exacerbations. In: Chronic Obstructive Pulmonary Disease Exacerbations. Wedzicha JA & Martinez FJ (eds). Informa UK Ltd 2008 pp 191-202.
Walton R, Bartlett N, Stanciu L, et al., 2008, Viral modification of allergen responses in the airway, 27th Congress of the European-Academy-of-Allergology-and-Clinical-Immunology, Publisher: BLACKWELL PUBLISHING, Pages: 575-575, ISSN: 0105-4538
Sykes A, Mallia P, Johnston SL, 2007, Diagnosis of pathogens in exacerbations of chronic obstructive pulmonary disease., Proc Am Thorac Soc, Vol: 4, Pages: 642-646, ISSN: 1546-3222
Chronic obstructive pulmonary disease (COPD) is increasing in prevalence. Acute exacerbations of COPD are the major cause worldwide of morbidity, mortality, and health care costs as well as decreased quality of life for the individual. The majority of exacerbations are infectious in etiology. Bacteria are detected in 50% of exacerbations and polymerase chain reaction techniques have established that, in half to two-thirds of exacerbations, viruses are causative pathogens. Combined bacterial and viral infection can be identified in 25% of exacerbations and these dual infections are often more severe. Despite occurring frequently, the mechanisms by which infection with these pathogens causes exacerbations are incompletely understood. This highlights the need for continued research, because a greater understanding of the mechanism of COPD exacerbations may lead to identification of potential targets for the development of therapeutic options for this increasingly common condition.
Kamath AV, Monteiro WR, Mildenhall S, et al., 2007, A study of airway inflammation and viral infection in acute severe asthma, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: A129-A129, ISSN: 0040-6376
Wark PAB, Bucchieri F, Johnston SL, et al., 2007, IFN-gamma-induced protein 10 is a novel biomarker of rhinovirus-induced asthma exacerbations., J Allergy Clin Immunol, Vol: 120, Pages: 586-593, ISSN: 0091-6749
BACKGROUND: Rhinovirus-induced acute asthma is the most frequent trigger for asthma exacerbations. OBJECTIVE: We assessed which inflammatory mediators were released from bronchial epithelial cells (BECs) after infection with rhinovirus and then determined whether they were also present in subjects with acute virus-induced asthma, with the aim to identify a biomarker or biomarkers for acute virus-induced asthma. METHODS: BECs were obtained from bronchial brushings of steroid-naive asthmatic subjects and healthy nonatopic control subjects. Cells were infected with rhinovirus 16. Inflammatory mediators were measured by means of flow cytometry with a cytometric bead array. Subjects with acute asthma and virus infection were recruited; they were characterized clinically by using lung function tests and had blood taken to measure the inflammatory mediators identified as important by the BEC experiments. RESULTS: IFN-gamma-induced protein 10 (IP-10) and RANTES were released in the greatest quantities, followed by IL-6, IL-8, and TNF-alpha. Dexamethasone treatment of BECs only partially suppressed IP-10 and TNF-alpha but was more effective at suppressing RANTES, IL-6, and IL-8. In acute clinical asthma serum IP-10 levels were increased to a greater extent in those with acute virus-induced asthma (median of 604 pg/mL compared with 167 pg/mL in those with non-virus-induced acute asthma, P < .01). Increased serum IP-10 levels were predictive of virus-induced asthma (odds ratio, 44.3 [95% CI, 3.9-100.3]). Increased serum IP-10 levels were strongly associated with more severe airflow obstruction (r = -0.8; P < .01). CONCLUSIONS: IP-10 release is specific to acute virus-induced asthma. CLINICAL IMPLICATIONS: Measurement of serum IP-10 could be used to predict a viral trigger to acute asthma.
Wark PAB, Bucchieri F, Johnston SL, et al., 2007, IFN-γ-induced protein 10 is a novel biomarker of rhinovirus-induced asthma exacerbations, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 120, Pages: 586-593, ISSN: 0091-6749
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- Citations: 133
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
Papi A, Contoli M, Caramori G, et al., 2007, Models of infection and exacerbations in COPD (vol 7, pg 259, 2007), CURRENT OPINION IN PHARMACOLOGY, Vol: 7, Pages: 451-451, ISSN: 1471-4892
Johnston SL, 2007, Innate immunity in the pathogenesis of virus-induced asthma exacerbations., Proc Am Thorac Soc, Vol: 4, Pages: 267-270, ISSN: 1546-3222
The major asthma morbidity, mortality, and health care costs are a result of acute exacerbations. However, exacerbations are only partially responsive to current therapies and new approaches to treatment are needed. The great majority of acute asthma exacerbations are associated with respiratory viral infections and, of viruses implicated, approximately 60% are human rhinoviruses (RVs). The mechanisms of RV-induced asthma exacerbations are poorly understood. We have previously shown that adults with asthma have increased susceptibility to naturally occurring RV infections. Our recent studies have investigated mechanisms of innate host defense against RV infection. First, primary bronchial epithelial cells from subjects with asthma were shown to replicate RV in vitro to several logs, whereas those of normal control subjects were resistant to infection. This resistance was a result of rapid induction of apoptosis and of interferon (IFN)-beta in the normal cells, whereas these responses were deficient in asthmatic cells. These studies were recently extended to a novel family of three related proteins, the IFN-lambdas 1-3, production of which was also deficient in vitro and related to asthma exacerbation severity in vivo. These studies identify novel mechanisms for the increased susceptibility of subjects with asthma to RV infection. Further studies are now required to investigate whether administration of IFN-beta or IFN-lambda may be beneficial in the treatment of asthma exacerbations, to determine whether similar deficiencies are observed in children and in subjects with nonatopic asthma, and to investigate the mechanisms of deficient IFN production in asthma to help identify better therapeutic strategies for asthma exacerbations.
Johnston NW, Johnston SL, Norman GR, et al., 2007, The September epidemic of asthma hospitalization: School children as disease vectors (vol 117, pg 557, 2006), JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 120, Pages: 47-47, ISSN: 0091-6749
Papi A, Contoli M, Gaetano C, et al., 2007, Models of infection and exacerbations in COPD, CURRENT OPINION IN PHARMACOLOGY, Vol: 7, Pages: 259-265, ISSN: 1471-4892
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- Citations: 5
Kusel MMH, de Klerk NH, Kebadze T, et al., 2007, Early-life respiratory viral infections, atopic sensitization, and risk of subsequent development of persistent asthma, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 119, Pages: 1105-1110, ISSN: 0091-6749
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- Citations: 547
Papadopoulos NG, Xepapadaki P, Mallia P, et al., 2007, Mechanisms of virus-induced asthma exacerbations:: state-of-the-art.: A GA<SUP>2</SUP>LEN and InterAirways document, ALLERGY, Vol: 62, Pages: 457-470, ISSN: 0105-4538
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- Citations: 83
Blasi F, Johnston SL, 2007, The role of antibiotics in asthma, INTERNATIONAL JOURNAL OF ANTIMICROBIAL AGENTS, Vol: 29, Pages: 485-493, ISSN: 0924-8579
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- Citations: 31
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.
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