Forns D.,Autonomous University of Barcelona |
Prat R.,Autonomous University of Barcelona |
Tauler E.,Pediatric Allergy Unit
Allergologia et Immunopathologia | Year: 2011
Background: The health-related quality of life (HRQoL) of asthmatic children and their caregivers is correlated to management of the disease and the presence of certain morbidity indicators. The integral assessment of paediatric asthma must include the evaluation of HRQoL among the caregivers, although existing questionnaires only partially assess the dimensions of this aspect. The present study describes a new questionnaire for evaluating HRQoL among the caregivers, comprising three dimensions (functional, emotional, and socio-occupational). Material and methods: The study involves two phases. A total of 81 patients between 3 and 9 years of age and their caregivers participated in the first phase, involving a qualitative and psychometric study of the preliminary version of the questionnaire (IFABI). A total of 137 patients between 2 and 17 years of age and their caregivers participated in the second phase, in which the revised version of the questionnaire (IFABI-R) was developed and subjected to psychometric evaluation. Results: First phase: The IFABI showed important reliability and internal consistency (Cronbach alpha=0.93), concurrent validity requiring improvement, and a scantly clear internal structure. Second phase: The IFABI-R showed important reliability and internal consistency (Cronbach alpha=0.90), adequate concurrent validity, and a three-dimensional structure whose three factors correspond to the three dimensions of the questionnaire. Conclusions: The good psychometric results obtained with the IFABI-R justify its use in paediatric asthmatic patients. The questionnaire is currently being scaled, and its sensitivity to change is being assessed. © 2010 SEICAP. Source
Papadopoulos N.G.,National and Kapodistrian University of Athens |
Christodoulou I.,National and Kapodistrian University of Athens |
Rohde G.,Maastricht University |
Agache I.,Transylvania University |
And 37 more authors.
Allergy: European Journal of Allergy and Clinical Immunology | Year: 2011
A major part of the burden of asthma is caused by acute exacerbations. Exacerbations have been strongly and consistently associated with respiratory infections. Respiratory viruses and bacteria are therefore possible treatment targets. To have a reasonable estimate of the burden of disease induced by such infectious agents on asthmatic patients, it is necessary to understand their nature and be able to identify them in clinical samples by employing accurate and sensitive methodologies. This systematic review summarizes current knowledge and developments in infection epidemiology of acute asthma in children and adults, describing the known impact for each individual agent and highlighting knowledge gaps. Among infectious agents, human rhinoviruses are the most prevalent in regard to asthma exacerbations. The newly identified type-C rhinoviruses may prove to be particularly relevant. Respiratory syncytial virus and metapneumovirus are important in infants, while influenza viruses seem to induce severe exacerbations mostly in adults. Other agents are relatively less or not clearly associated. Mycoplasma and Chlamydophila pneumoniae seem to be involved more with asthma persistence rather than with disease exacerbations. Recent data suggest that common bacteria may also be involved, but this should be confirmed. Although current information is considerable, improvements in detection methodologies, as well as the wide variation in respect to location, time and populations, underline the need for additional studies that should also take into account interacting factors. © 2010 John Wiley & Sons A/S. Source
Chavali S.,University of Cambridge |
Bruhn S.,Linkoping University |
Tiemann K.,Linkoping University |
Saetrom P.,Norwegian University of Science and Technology |
And 7 more authors.
RNA | Year: 2013
MicroRNAs (miRNAs) play a key role in regulating mRNA expression, and individual miRNAs have been proposed as diagnostic and therapeutic candidates. The identification of such candidates is complicated by the involvement of multiple miRNAs and mRNAs as well as unknown disease topology of the miRNAs. Here, we investigated if disease-associated miRNAs regulate modules of disease-associated mRNAs, if those miRNAs act complementarily or synergistically, and if single or combinations of miRNAs can be targeted to alter module functions. We first analyzed publicly available miRNA and mRNA expression data for five different diseases. Integrated target prediction and network-based analysis showed that the miRNAs regulated modules of disease-relevant genes. Most of the miRNAs acted complementarily to regulate multiple mRNAs. To functionally test these findings, we repeated the analysis using our own miRNA and mRNA expression data from CD4+ T cells from patients with seasonal allergic rhinitis. This is a good model of complex diseases because of its well-defined phenotype and pathogenesis. Combined computational and functional studies confirmed that miRNAs mainly acted complementarily and that a combination of two complementary miRNAs, miR-223 and miR-139-3p, could be targeted to alter disease-relevant module functions, namely, the release of type 2 helper T-cell (Th2) cytokines. Taken together, our findings indicate that miRNAs act complementarily to regulate modules of disease-related mRNAs and can be targeted to alter disease-relevant functions. Source
Wang H.,Gothenburg University |
Mobini R.,Gothenburg University |
Fang Y.,Gothenburg University |
Fang Y.,Affiliated Hospital of Guiyang Medical College |
And 6 more authors.
Clinical and Experimental Allergy | Year: 2010
Background Previously, expression profiling has been used to analyse allergen-challenged T-helper type 2 cells, nasal biopsies and nasal fluid cells from patients with seasonal allergic rhinitis (SAR). Allergen-challenged peripheral blood mononuclear cells (PBMCs) provide a human in vitro model of how antigen-presenting cells, CD4 + T cells and effector cells such as basophils interact in allergic inflammation. Objective To identify novel genes and pathways in allergen-challenged PBMCs from patients with SAR using gene expression profiling and functional studies. Methods PBMCs from 11 patients with SAR and 23 healthy controls were analysed with gene expression profiling. mRNA expression of IL17RB in basophils was evaluated using quantitative real-time PCR. Membrane protein expression and apoptosis of basophils were examined by flow cytometry. Degranulation of basophils was assessed by measuring β-hexosaminidase release. Cytokine release was measured using ELISA. Results Gene expression microarray analysis of allergen-challenged PBMCs showed that 209 out of 44 000 genes were differentially expressed in patients compared with controls. IL17RB was the gene whose expression increased most in patients (P<0.0001). FACS analysis of PBMCs showed, for the first time, that basophils express IL-17RB. Following allergen challenge, IL-17RB protein increased significantly on basophils from patients compared with controls (P<0.05). IL-3 significantly increased both mRNA and protein expressions of IL17RB. Activation of IL-17RB by its ligand, IL-25, inhibited apoptosis of basophils. Moreover, IgE-mediated degranulation was enhanced by IL-25. Conclusion Increased expression of IL-17RB on allergen-challenged basophil is regulated by IL-3, inhibits apoptosis and promotes IgE-mediated degranulation of basophils. © 2010 Blackwell Publishing Ltd. Source
Cipriani F.,University of Bologna |
Ricci G.,University of Bologna |
Leoni M.C.,University of Pavia |
Capra L.,University of Ferrara |
And 4 more authors.
Journal of Dermatology | Year: 2014
The idea that a mechanism of autoimmunity could play a role in the pathogenesis of atopic dermatitis gained support from the observation that patients with atopic dermatitis display IgE reactivity to a variety of human protein antigens, several of which have been characterized at molecular level. A broad spectrum of at least 140 IgE-binding self-antigens associated with atopic dermatitis has been demonstrated; they might promote, perpetuate, or both, skin inflammation by binding IgE antibodies or activating specific T cells. Even if the presence of autoreactivity seems to be associated with the severity of the disease and may be used as a parameter reflecting chronic tissue damage, at the state of art the role of autoimmunity in atopic dermatitis is far from clear. Data from the literature show that the use of autoantibodies as biomarkers of atopic dermatitis are still limited by the evidence that the epiphenomenon of autoreactivity is detectable only in a percentage of patients and that the involved self-allergens often are not the same; further longitudinal case-control studies are needed to investigate and to clarify the pathogenethic role of autoimmunity in the course of atopic dermatitis. © 2014 Japanese Dermatological Association. Source