J. Mullol
Instituto de Salud Carlos III
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Featured researches published by J. Mullol.
Clinical & Experimental Allergy | 2006
A. Martínez‐Antón; C. DeBolós; M. Garrido; Roca-Ferrer J; C. Barranco; Isam Alobid; Antoni Xaubet; César Picado; J. Mullol
Background Mucus hyper‐secretion is a feature of several airways diseases such as chronic rhinosinusitis, asthma, and cystic fibrosis (CF). Since mucins are major components of mucus, the knowledge of their distribution and regulation in nasal tissues is likely to improve mucus hyper‐secretion therapy.
Allergy | 2004
Laura Pujols; J. Mullol; Alfons Torrego; César Picado
Inhaled and intranasal glucocorticoids are the most common and effective drugs for controlling symptoms and airway inflammation in respiratory diseases such as asthma, allergic rhinitis, and nasal polyposis. The last few years have seen a growing understanding of the mechanisms of glucocorticoid action and, in particular, the receptor that mediates glucocorticoid actions, the glucocorticoid receptor (GR). In this revision we present an update on the GR gene, the expression and regulation of its gene products, namely GRα and GRβ, as well as their alterations in pathological states. GRα is responsible for the induction and repression of target genes, it is expressed in virtually all human cells and tissues, and its expression is known to be downregulated by glucocorticoids. GRβ has been found to act as a dominant negative inhibitor of GRα‐mediated transactivation in in vitro studies with transfected cells, but it does not appear to have a significant inhibitory effect on GRα‐mediated transrepression. In addition, for most tissues the expression of GRβ, at least at the mRNA level, is extremely low compared with that of GRα. Some pro‐inflammatory cytokines appear to upregulate the expression of GRβ, and increased GRβ expression has been reported in diseases associated with glucocorticoid resistance or insensitivity, such as bronchial asthma, nasal polyposis, and ulcerative colitis. However, the possible role of GRβ in modulating glucocorticoid sensitivity and/or resistance in vivo has been highly debated and it is not yet clear.
Clinical & Experimental Allergy | 1994
Antoni Xaubet; J. Mullol; E. López; Roca-Ferrer J; M. Rozman; T. Carriön; J. M. Fabra; César Picado
Eosinophilic infiltration of the respiratory mucosa is considered an inflammatory hallmark of allergic rhinitis, bronchial asthma and nasal polyposis. However, the mechanisms involved in this infiltration have not yet been totally elucidated. The objective of this study was to investigate and compare the influence of epithelial cell secretions from both nasal polyps (NP) and normal nasal mucosa (NM) on in vitro eosinophil survival. Epithelial cells were identified by microscopy; and immunohislochemisiry. cultured to confluence, and human epithelial cell conditioned media (HECM) was generated from cultures. Eosinophits were isolated at high viability and purity (>90%) from peripheral blood and incubated with HECM. HECM from both NM and NP increased eosinophil survival in a dose‐dependent manner, this effect being maximal at a concentration of 25% for NM (73.4%±5.5%, n= 26, P< 0.001) and of 10% for NP (74.5%± 84%n= 18, P < 0.001). Incubation of monoclonal antibody to human GM‐CSF with HECM, neutralized the induction of eosinophil survival by HECM from both NM and NP. HECM from NP contained higher concentrations of GM‐CSF (111 ± 25.4 pg/ml, n= 17) than HECM from NM (97.1 ± 15.2 pg/ml. n= 8). without reaching statistical significance. Pre‐incubation of dexamethasone with eosinophils also blocked HFCM‐induced eosinophil survival from both NM (10−8‐10−5 M; IC50 = 9.5 nM) and NP (10‐7‐10‐5 M; IC50 = 83 nM). These results suggest that: firstly eosinophil infiltration into the respiratory mucosa during allergic reaction and nasal polyposis may be modulated at least in part by GM‐CSF from epithelial cells; and secondly epithelial cells from NP might have a more potent effect on inducing eosinophil infiltration of the respiratory mucosa than epithelial cells from NM. Finally, we may consider this as a reliable in vitro model to compare the role of epithelial cells from inflammatory (NP) and non‐inflammatory (NM) tissue in respiratory inflammation.
Allergy | 2008
Isam Alobid; Manuel Bernal-Sprekelsen; J. Mullol
Chronic rhinosinusitis (CRS) including nasal polyps is a chronic inflammatory disease of the nasal and paranasal sinus mucosa that, despite differing hypotheses of its cause, remains poorly understood. Primary symptoms are nasal blockage, loss of smell, rhinorrhea, and facial pain or pressure. Chronic rhinosinusitis causes significant physical symptoms, has a negative impact on quality of life (QoL), and can substantially impair daily functioning. A global evaluation of patients must include, together with nasal symptoms, nasal endoscopy, and CT scan, the measurement of QoL. To assess QoL in CRS, specific and generic questionnaires may be used. Chronic rhinosinusitis has a considerable impact on a patient’s QoL but comorbidities, such as asthma and atopy, have an accumulative negative effect. Both medical and surgical treatments lead to a similar improvement on the QoL of CRS and nasal polyp patients.
European Respiratory Journal | 1997
Roca-Ferrer J; J. Mullol; E. López; Antoni Xaubet; Laura Pujols; Jc Fernandez; César Picado
Topical anti-inflammatory drugs decrease eosinophil infiltration. This action may be due to an effect on the release of epithelial cell products responsible for promoting eosinophil survival. We investigated the effect of fluticasone propionate, budesonide, beclomethasone dipropionate and nedocromil sodium on the release of granulocyte/macrophage colony-stimulating factor (GM-CSF) and on eosinophil survival induced by secretions from cultured nasal epithelial cells. Human epithelial cell-conditioned media (HECM) were generated by cultured epithelial cells obtained from healthy subjects undergoing corrective nasal surgery. Normodense eosinophils isolated from peripheral blood were incubated with HECM generated with and without the drugs. All of the drugs tested inhibited eosinophil survival, and response was dose-dependent. Fluticasone propionate had the highest inhibitory potency (25% inhibitory concentration (IC25) 1x10(-9) M), followed by budesonide (IC25 3.3x10(-8) M), beclomethasone dipropionate (IC25 1.5x10(-6) M), and nedocromil sodium IC25 5x10(-6) M). Likewise, fluticasone was the strongest steroid in inhibiting release of GM-CSF (IC25 8.4x10(-11) M), followed by budesonide (IC25 2x10(-9) M), beclomethasone dipropionate (IC25 13x10(-8) M), and nedocromil sodium (IC25 >10(-5) M). A significant correlation was found between both inhibitory effects (r=0.955; p<0.05). Topical anti-inflammatory drugs may decrease eosinophil survival by abrogating the promoting effect of epithelial cells. These drugs may exert part of their therapeutic effect by modulating GM-CSF release. The following rank of potency was observed: fluticasone propionate > budesonide > beclomethasone dipropionate > nedocromil sodium. The study of the interaction between epithelial cells and eosinophils may be a useful method for investigating and comparing the potency of topical drugs.
Allergy | 2009
Jose Maria Guilemany; J. Angrill; Isam Alobid; Silvia Centellas; Laura Pujols; Joan Bartra; Manuel Bernal-Sprekelsen; Antonio Valero; César Picado; J. Mullol
Background:u2002 Although various relationships between the lower and upper airways have been found, the association of bronchiectasis with chronic rhinosinusitis and nasal polyps has not been thoroughly evaluated. This study was undertaken to examine the association of idiopathic and postinfective bronchiectasis with chronic rhinosinusitis and nasal polyposis.
Clinical & Experimental Allergy | 1997
J. Mullol; E. López; Roca-Ferrer J; Antoni Xaubet; Laura Pujols; Joan C. Fernàndez-Morata; J. M. Fabra; César Picado
Background Eosinophil infiltration is a hallmark of the inflammatory response in rhinitis and in nasal polypcsis.
Clinical & Experimental Allergy | 2000
Joan C. Fernàndez-Morata; J. Mullol; Mireya Fuentes; Laura Pujols; Roca-Ferrer J; Pérez M; Antoni Xaubet; César Picado
Cyclooxygenase (COX) converts arachidonic acid in prostanoids. COX exists in two isoforms, COX‐1 is the constitutive whereas COX‐2 is the inducible isoform. The regulation of COX‐1 and COX‐2 expression in nasal mucosa has not been previously reported.
Allergy | 2009
Jose Maria Guilemany; J. Angrill; Isam Alobid; Silvia Centellas; E. Prades; J. Roca; Laura Pujols; Manuel Bernal-Sprekelsen; César Picado; J. Mullol
Background:u2002 The nose and the bronchi belong, in anatomical and physiopathological terms, to the concept of united airways. Associations between upper and lower airways diseases have been demonstrated in allergic rhinitis and asthma, nasal polyposis (NP) and asthma, chronic rhinosinusitis (CRS) and chronic obstructive pulmonary disease, and more recently CRS/NP and bronchiectasis (BQ).
Clinical & Experimental Allergy | 2006
J. Mullol; Roca-Ferrer J; Isam Alobid; Laura Pujols; Antonio Valero; Antoni Xaubet; Manuel Bernal-Sprekelsen; César Picado
Background Second‐generation antihistamines are H1 receptor antagonists and may have additional anti‐inflammatory effects.