546 results found
Ching Y-M, Edwards MR, Glanville N, et al., 2014, Innate Type I Interferon Signalling Modulates Th2 Responses In Mouse Models Of Rhinovirus-Induced Airways Disease, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 189, ISSN: 1073-449X
Stavrou A, Jolly L, Glanville N, et al., 2014, Influenza Infection, But Not Rhinovirus Infection, May Cause Exacerbation Of Lung Fibrosis Through Lung Collagen Deposition, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 189, ISSN: 1073-449X
Peel TJ, Jackson DJ, Johnston SL, et al., 2014, Il-23, Increased In Asthmatics, Licences Il-17 Secretion In Response To Rhinovirus Infection, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 189, ISSN: 1073-449X
Brignull LM, Czimmerer Z, Saidi H, et al., 2013, Reprogramming of lysosomal gene expression by interleukin-4 and Stat6, BMC Genomics, Vol: 14, ISSN: 1471-2164
BackgroundLysosomes play important roles in multiple aspects of physiology, but the problem of how the transcription of lysosomal genes is coordinated remains incompletely understood. The goal of this study was to illuminate the physiological contexts in which lysosomal genes are coordinately regulated and to identify transcription factors involved in this control.ResultsAs transcription factors and their target genes are often co-regulated, we performed meta-analyses of array-based expression data to identify regulators whose mRNA profiles are highly correlated with those of a core set of lysosomal genes. Among the ~50 transcription factors that rank highest by this measure, 65% are involved in differentiation or development, and 22% have been implicated in interferon signaling. The most strongly correlated candidate was Stat6, a factor commonly activated by interleukin-4 (IL-4) or IL-13. Publicly available chromatin immunoprecipitation (ChIP) data from alternatively activated mouse macrophages show that lysosomal genes are overrepresented among Stat6-bound targets. Quantification of RNA from wild-type and Stat6-deficient cells indicates that Stat6 promotes the expression of over 100 lysosomal genes, including hydrolases, subunits of the vacuolar H+ ATPase and trafficking factors. While IL-4 inhibits and activates different sets of lysosomal genes, Stat6 mediates only the activating effects of IL-4, by promoting increased expression and by neutralizing undefined inhibitory signals induced by IL-4.ConclusionsThe current data establish Stat6 as a broadly acting regulator of lysosomal gene expression in mouse macrophages. Other regulators whose expression correlates with lysosomal genes suggest that lysosome function is frequently re-programmed during differentiation, development and interferon signaling.
Molyneaux PL, Cox MJ, Mallia P, et al., 2013, THE ROLE OF THE RESPIRATORY MICROBIOME IN IDIOPATHIC PULMONARY FIBROSIS, Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A22-A22, ISSN: 0040-6376
Footitt J, Mallia P, Durham A, et al., 2013, HDAC ACTIVITY IN MACROPHAGES IN EXPERIMENTAL RHINOVIRUS INFECTION IN COPD, Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A58-A59, ISSN: 0040-6376
Custovic A, Johnston SL, Pavord I, et al., 2013, EAACI position statement on asthma exacerbations and severe asthma, ALLERGY, Vol: 68, Pages: 1520-1531, ISSN: 0105-4538
van der Sluijs KF, van de Pol MA, Kulik W, et al., 2013, Systemic tryptophan and kynurenine catabolite levels relate to severity of rhinovirus-induced asthma exacerbation: a prospective study with a parallel-group design, THORAX, Vol: 68, Pages: 1122-1130, ISSN: 0040-6376
Molyneaux PL, Mallia P, Cox MJ, et al., 2013, Outgrowth of the Bacterial Airway Microbiome after Rhinovirus Exacerbation of Chronic Obstructive Pulmonary Disease, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 188, Pages: 1224-1231, ISSN: 1073-449X
de Souza Alves CC, Collison A, Hatchwell L, et al., 2013, Inhibiting AKT Phosphorylation Employing Non-Cytotoxic Anthraquinones Ameliorates T(H)2 Mediated Allergic Airways Disease and Rhinovirus Exacerbation, PLOS ONE, Vol: 8, ISSN: 1932-6203
Papi A, Contoli M, Adcock IM, et al., 2013, Rhinovirus infection causes steroid resistance in airway epithelium through nuclear factor kappa B and c-Jun N-terminal kinase activation, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 132, Pages: 1075-+, ISSN: 0091-6749
Glanville N, Message SD, Walton RP, et al., 2013, gamma delta T cells suppress inflammation and disease during rhinovirus-induced asthma exacerbations, MUCOSAL IMMUNOLOGY, Vol: 6, Pages: 1091-1100, ISSN: 1933-0219
Drysdale SB, Alcazar-Paris M, Wilson T, et al., 2013, Rhinovirus infection and healthcare utilisation in prematurely born infants, EUROPEAN RESPIRATORY JOURNAL, Vol: 42, Pages: 1029-1036, ISSN: 0903-1936
Vareille M, Kieninger E, Alves MP, et al., 2013, Impaired type I and type III interferon induction and rhinovirus control in human cystic fibrosis airway epithelial cells (Retraction of 67, 517, 2012), THORAX, Vol: 68, Pages: 886-886, ISSN: 0040-6376
Glanville N, Mclean GR, Guy B, et al., 2013, Cross-Serotype Immunity Induced by Immunization with a Conserved Rhinovirus Capsid Protein, PLOS PATHOGENS, Vol: 9, ISSN: 1553-7374
Porter JD, Macintyre J, Sykes A, et al., 2013, Azithromycin is able to augment interferon and interferon stimulated gene responses to rhinovirus in vitro, World Allergy and Asthma Congress of the European-Academy-of-Allergy-and-Clinical-Immunology and World-Allergy-Organization, Publisher: WILEY-BLACKWELL, Pages: 300-300, ISSN: 0105-4538
Khaitov M, Nikonova A, Jackson D, et al., 2013, The role of M1 and M2 macrophages during rhinovirus-induced asthma exacerbation, World Allergy and Asthma Congress of the European-Academy-of-Allergy-and-Clinical-Immunology and World-Allergy-Organization, Publisher: WILEY-BLACKWELL, Pages: 56-56, ISSN: 0105-4538
Traub S, Nikonova A, Carruthers A, et al., 2013, An Anti-Human ICAM-1 Antibody Inhibits Rhinovirus-Induced Exacerbations of Lung Inflammation, PLOS PATHOGENS, Vol: 9, ISSN: 1553-7366
Mallia P, Message SD, Contoli M, et al., 2013, Neutrophil adhesion molecules in experimental rhinovirus infection in COPD, Respiratory Research, Vol: 14, ISSN: 1465-993X
BackgroundCOPD exacerbations are associated with neutrophilic airway inflammation. Adhesion molecules on the surface of neutrophils may play a key role in their movement from blood to the airways. We analysed adhesion molecule expression on blood and sputum neutrophils from COPD subjects and non-obstructed smokers during experimental rhinovirus infections.MethodsBlood and sputum were collected from 9 COPD subjects and 10 smoking and age-matched control subjects at baseline, and neutrophil expression of the adhesion molecules and activation markers measured using flow cytometry. The markers examined were CD62L and CD162 (mediating initial steps of neutrophil rolling and capture), CD11a and CD11b (required for firm neutrophil adhesion), CD31 and CD54 (involved in neutrophil transmigration through the endothelial monolayer) and CD63 and CD66b (neutrophil activation markers). Subjects were then experimentally infected with rhinovirus-16 and repeat samples collected for neutrophil analysis at post-infection time points.ResultsAt baseline there were no differences in adhesion molecule expression between the COPD and non-COPD subjects. Expression of CD11a, CD31, CD62L and CD162 was reduced on sputum neutrophils compared to blood neutrophils. Following rhinovirus infection expression of CD11a expression on blood neutrophils was significantly reduced in both subject groups. CD11b, CD62L and CD162 expression was significantly reduced only in the COPD subjects. Blood neutrophil CD11b expression correlated inversely with inflammatory markers and symptom scores in COPD subjects.ConclusionFollowing rhinovirus infection neutrophils with higher surface expression of adhesion molecules are likely preferentially recruited to the lungs. CD11b may be a key molecule involved in neutrophil trafficking in COPD exacerbations.
Majoor CJ, Kamphuisen PW, Van de Pol MA, et al., 2013, Rhinovirus infection induces procoagulant changes in parallel with eosinophilic airway inflammation, JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Vol: 11, Pages: 742-742, ISSN: 1538-7933
Kupczyk M, Haque S, Sterk PJ, et al., 2013, Detection of exacerbations in asthma based on electronic diary data: results from the 1-year prospective BIOAIR study, THORAX, Vol: 68, Pages: 611-618, ISSN: 0040-6376
Almond MH, Edwards MR, Barclay WS, et al., 2013, Obesity and susceptibility to severe outcomes following respiratory viral infection, THORAX, Vol: 68, Pages: 684-686, ISSN: 0040-6376
Edwards MR, Regamey N, Vareille M, et al., 2013, Impaired innate interferon induction in severe therapy resistant atopic asthmatic children, MUCOSAL IMMUNOLOGY, Vol: 6, Pages: 797-806, ISSN: 1933-0219
Sykes A, Edwards MR, Macintyre J, et al., 2013, TLR3, TLR4 and TLRs7-9 Induced Interferons Are Not Impaired in Airway and Blood Cells in Well Controlled Asthma, PLOS One, Vol: 8, ISSN: 1932-6203
Defective Rhinovirus induced interferon-β and interferon-λ production has been reported in bronchial epithelial cells from asthmatics but the mechanisms of defective interferon induction in asthma are unknown. Virus infection can induce interferon through Toll like Receptors (TLR)3, TLR7 and TLR8. The role of these TLRs in interferon induction in asthma is unclear. This objective of this study was to measure the type I and III interferon response to TLR in bronchial epithelial cells and peripheral blood cells from atopic asthmatics and non-atopic non-asthmatics. Bronchial epithelial cells and peripheral blood mononuclear cells from atopic asthmatic and non-atopic non-asthmatic subjects were stimulated with agonists to TLR3, TLR4 & TLRs7–9 and type I and III interferon and pro-inflammatory cytokine, interleukin(IL)-6 and IL-8, responses assessed. mRNA expression was analysed by qPCR. Interferon proteins were analysed by ELISA. Pro-inflammatory cytokines were induced by each TLR ligand in both cell types. Ligands to TLR3 and TLR7/8, but not other TLRs, induced interferon-β and interferon-λ in bronchial epithelial cells. The ligand to TLR7/8, but not those to other TLRs, induced only type I interferons in peripheral blood mononuclear cells. No difference was observed in TLR induced interferon or pro-inflammatory cytokine production between asthmatic and non-asthmatic subjects from either cell type. TLR3 and TLR7/8,, stimulation induced interferon in bronchial epithelial cells and peripheral blood mononuclear cells. Interferon induction to TLR agonists was not observed to be different in asthmatics and non-asthmatics.
Mallia P, Singanayagam A, Johnston SL, 2013, Virus-bacteria interactions in COPD exacerbations, European Respiratory Monograph, Vol: 60, Pages: 76-83, ISSN: 1025-448X
Chronic obstructive pulmonary disease (COPD) is a disease characterised by acute exacerbations. Respiratory infections, including viruses and bacteria, are common aetiological agents and some studies have detected dual viral- bacterial infection during exacerbations. However, the mechanisms underlying virus-bacteria interactions in COPD are poorly characterised. In vitro studies have shown that viral infection can increase susceptibility to secondary bacterial infection, and animal models of sequential infection have revealed potential molecular mechanisms of how viral infection may impact upon subsequent secondary bacterial infection. A recently reported human experimental rhinovirus infection model of COPD exacerbation has provided additional evidence that viral- bacterial co-infection may be more common in COPD exacerbations than previously thought. Further understanding of the mechanisms involved in virus-bacteria interactions may facilitate development of novel therapies with the potential to reduce or prevent secondary bacterial infections following respiratory viral exacerbations in COPD. In this chapter, the evidence for dual viral and bacterial infection in COPD exacerbations is outlined, and existing evidence for underlying mechanistic interactions is discussed. © ERS 2013.
Dhariwal J, Edwards MR, Johnston SL, 2013, Anti-viral agents: potential utility in exacerbations of asthma, CURRENT OPINION IN PHARMACOLOGY, Vol: 13, Pages: 331-336, ISSN: 1471-4892
Foster PS, Plank M, Collison A, et al., 2013, The emerging role of microRNAs in regulating immune and inflammatory responses in the lung, IMMUNOLOGICAL REVIEWS, Vol: 253, Pages: 198-215, ISSN: 0105-2896
Bardin PG, Johnston SL, Hamilton G, 2013, Middle airway obstruction-it may be happening under our noses, THORAX, Vol: 68, Pages: 396-398, ISSN: 0040-6376
Hatchwell L, Collison A, Phipps S, et al., 2013, CCL7 (MCP-3) MEDIATES RHINOVIRUS-INDUCED LUNG INFLAMMATION AND EXACERBATION OF ALLERGIC AIRWAY DISEASE, RESPIROLOGY, Vol: 18, Pages: 40-40, ISSN: 1323-7799
Girkin J, Hatchwell L, Foster PS, et al., 2013, SALMETEROL ATTENUATES CHEMOTAXIS IN RHINOVIRUS-INDUCED EXACERBATION OF ASTHMA VIA MODULATION OF PP2A, RESPIROLOGY, Vol: 18, Pages: 13-13, ISSN: 1323-7799
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