Background Most patients with nonallergic asthma have normal serum immunoglobulin E (IgE) levels. Recent reports suggest that total and aeroallergen-specific IgE levels in induced sputum may be higher in nonallergic asthmatics than in healthy controls. Our objective is to compare total and dust-mite specific (Der p 1) IgE levels in induced sputum in allergic and nonallergic asthmatics and healthy controls. Methods Total and Der p 1-specific IgE were measured in induced sputum (ImmunoCAP immunoassay) from 56 age- and sex-matched asthmatics (21 allergic, 35 nonallergic) and 9 healthy controls. Allergic asthma was defined as asthma with a positive prick test and/or clinically-significant Der p 1-specific serum IgE levels. Results Patients with allergic asthma presented significantly higher total and Der p 1-specific serum IgE levels. There were no significant between-group differences in total sputum IgE. However, Der p 1-specific sputum IgE levels were significantly higher (p = 0.000) in the allergic asthmatics, but without differences between the controls and nonallergic asthmatics. Serum and sputum IgE levels were significantly correlated, both for total IgE (rho = 0.498; p = 0.000) and Der p 1-specific IgE (rho, 0.621; p = 0001). Conclusions Total IgE levels measured in serum and induced sputum are significantly correlated. No significant differences were found between the differents groups in total sputum IgE. Nevertheless, the levels of Der p 1-specific sputum IgE levels were significantly higher in the allergic asthmatics, but without differences between the controls and nonallergic asthmatics. Probably due to the lack of sensitivity of the test used, but with the growing evidence for local allergic reactions better methods are need to explore its presence. The Clinical Trials Identifier for this project is NCT03640936.

Introduction: Antigen-specific CD4+ T cells induce airway smooth muscle (ASM) remodeling through direct contact. Mesenchymal stem cells (MSCs) may offer therapeutic potential for asthma but it is necessary to understand their immunomodulatory mechanisms and mediators. Aims and objectives: To test if MSCs, whether through direct contact or mediators, inhibit ASM cell proliferation in a CD4+ T cell/ASM co-culture model. Methods: Sprague-Dawley rats were intranasally exposed to D. pteronyssinus (HDM) with staphylococcal enterotoxin B, 3 times/week for 5 weeks. CD4+ T cells were harvested, HDM-activated and co-cultured with purified ASM cells plus adipose-derived MSCs, in direct contact or separated by a Transwell membrane. ASM cell proliferation was measured by flow-cytometry detection of 5-Etinyl-29-desoxyuridine (EdU) incorporation. Results: MSCs separated by Transwell were suppressive on CD4+ T cell-induced ASM proliferation in a dose-response fashion. EdU+ ASM cells were (Transwell versus direct contact) 23,68% vs 41,8% and 19,51% vs 41,8%, P<0.05, for 1:10 and 1:5 MSC:T-cell ratios respectively. Conclusions: MSCs inhibit CD4+ T cell-induced ASM cell proliferation through soluble mediators in a dose-response fashion. The identification of such mediators may contribute novel therapeutic agents for airway remodeling.

Patients often feel that their experience of illness is not valued nor understood by others. However, there has been a growing recognition of the importance of the patient perspective and involvement in research, improving its methodology and outcomes. The European Medicines Agency has been involving patients9 and consumers9 representatives on their work since 2005. The “European League Against Rheumatism recommendations for the inclusion of patient representatives in scientific projects” have been published in the “Annals of the rheumatic diseases” in 2011. I was diagnosed with Juvenile Idiopathic Arthritis when I was 5 years old, back in 1977. Therefore, I have 40 years of experience of living with a Rheumatic and Musculoskeletal Disease (RMD), but no recollection of what my life was like “before” and “after” the diagnosis. I have learned to live and cope with my RMD, with a sense of being different from my peers. This sense of “uniqueness” was only disrupted when I realised that my experience of illness was quite common to other persons with a RMD. I can still remember my fascination, in a Patient Reported Outcomes workshop, by discovering that our experience as patients had a bigger relevance that the one we usually conceive. Then, I felt the need of understanding the research process and specific jargon, so I could relate them with my knowledge on living with a RMD. Otherwise, any insight on the patient perspective would be “lost in translation”, due to an inability to establish a correspondence between the scientific terminology and mindset regarding the disease, and the experience of illness and sickness by the individuals. Training opportunities were also recognised as desirable by the above mentioned EULAR recommendations, to increase expertise and understanding of research methods and to promote the patients9 self-confidence on their contribution to research. The Patient Research Partners (PRP) training by EULAR, in 2013, was the first step towards a better understanding of what could be the role of patients and on how to provide a meaningful input from the patients9 perspective into research processes. It was followed in 2014 by the training provided by European Patients9 Academy on Therapeutic Innovation (EUPATI) for Patient Expert on the Medicines Research and Development Process. This expert-level training was organized in a mixture of independent e-learning coursework and face-to-face training events over a 14-month period. The syllabus involved six modules: Discovery of Medicines & Planning of Medicine Development, Non-Clinical Testing and Pharmaceutical Development, Exploratory and Confirmatory Clinical Development, Clinical Trials, Regulatory Affairs, Medicinal Product Safety, Pharmacovigilance and Pharmaco-epidemiology, HTA principles and practices. Additionally, in 2016, I have attended the 1st EULAR course on Health Economics in Rheumatology. In the meantime, my background as an anthropologist led me to become interested in Medical Anthropology. Between 2007–2015 my academic research (MA Phil. and PhD) was oriented towards a specialization in Anthropology of Health, with a special interest in Anthropology of Pharmaceuticals. Based on my personal experience, on this lecture I will focus on the challenges of the role of the PRP trying to fill the gap between the mindsets and practices of different stakeholders. Navigating through different meanings of symptoms and treatments, the educated patient representative must act like a translator, decodifying the biologic impact of the disease and intervention over the experience of illness on the everyday aspects of living with a RMD. The biggest expectation and challenge might be to bring these aspects forward, as relevant for the other stakeholders, since they shape individual values and patient9s preferences. Although recognised as having a pivotal role, patient9s involvement in research may be limited by tokenism or by ineffective patients9 participation. Patients9 involvement is now a requirement and an added value to any project. But, is the project team ready and willing to listen to patients? Are PRP duly involved in the project, or are they just expected to be recipients without any input of their perspectives into the development and implementation of the research? The knowledge and education acquired to perform our task enables us to understand science enough to communicate the patient experience in a meaningful way, improving the research. Our added value is, undoubtedly, our experience with the disease, our understanding of the individual values and preferences shaped by the everyday aspects of living with a RMD. We should be taken more seriously, for the benefit of science and patients. Disclosure of Interest None declared

Background In Portugal, the National Health Plan for 2012–2016 (1) and its extension to 2020 (2) consider citizenship-based strategies, including the involvement of patients/citizens and their representatives, as a key strategic axis to maximize health gains. However, actual policy initiatives and concrete actions have been limited to a couple initiatives without significant patient or public involvement. On the other side, several patient and citizen organizations (3–6) have been advocating for increased and meaningful involvement in health decision-making. Objectives To develop a Charter for Public Involvement in Health that is widely accepted and recognized by health stakeholders. Methods A working group was established with representatives from 13 patient organizations, 1 consumer organization and a research centre. A participatory action research methodology was used. The draft Charter was circulated for review and signature amongst more than 200 non-for-profit health-related organizations and over 50 key individuals publicly renowned for their work in health or public participation. The final version of the Charter was discussed with political and health stakeholders in a Forum held at the Portuguese parliament. Results A Charter for Public Involvement in Health, including the principles, scope, guidelines and means of participation was developed. In January 2017, 30 individuals (former and current political decision-makers, health care professionals, researchers and patients) and more than 82 non-for-profit health-related organizations (the majority being Portuguese disease-specific patient organizations) had signed the Charter. The conclusions of the Forum show that the Charter was recognized as a very important initiative to promote public involvement in health in Portugal. Challenges and barriers to further advancing patient and public engagement were also identified (e.g. political will, recognitions of patients as partners, patient empowerment, capacity-building, etc.). The Charter and the Forum were covered in the media and follow-up initiatives with health care professionals and hospital administrators are ongoing. Conclusions A patient-led Charter, developed by patient and consumer representatives, in collaboration with academia, and the public discussion with other health care stakeholders have proven successful to put public participation in the political and health care agenda. References Direção-Geral da Saúde – Ministério da Saúde. Plano Nacional de Saúde 2012–2016. Lisboa, Portugal; 2012. Direção-Geral da Saúde – Ministério da Saúde. Plano Nacional de Saúde – Revisão e Extensão a 2020. Lisboa, Portugal; 2015. European Patients Forum. The Value+ Policy Recommendations: Patient Involvement in Health Programmes and Policy [Internet]. Available from: http://www.eu-patient.eu/globalassets/projects/valueplus/doc_epf_policyrec.pdf. European Patients Forum. Patient Empowerment Campaign [Internet]. Available from: http://www.eu-patient.eu/campaign/PatientsprescribE/. International Alliance of Patients9 Organisations. Policy statement. Patient Involvement [Internet]. 2005. Available from: http://iapo.org.uk/sites/default/filesfiles/IAPO Policy Statement on Patient Involvement.pdf. Terzi A. The patients9 involvement in health policies in Europe. Roma; 2013. Disclosure of Interest S. Crisostomo Grant/research support from: Abbvie, Brustol-Meyers Squibb, Janssen, GSK, Pfizer, Roche and ViiV, M. Santos Grant/research support from: Abbvie, Brustol-Meyers Squibb, Janssen, GSK, Pfizer, Roche and ViiV, M. Serapioni: None declared, A. Matos: None declared, E. Mateus: None declared

Asthma with bronchial hypersecretion is a type of asthma that is poorly studied. Its pathogenesis is not well understood, but is probably related to innate impaired immunity, particularly with toll-like receptors (TLRs) and secretory mucins (MUC). OBJECTIVES:1) Define the clinical and inflammatory phenotype of asthma with bronchial hypersecretion of mucus. 2) Compare the type of mucin present in induced sputum (IS) of patients with and without bronchial hypersecretion. 3) Determine the expression of TLRs in IS and blood of asthmatics with and without bronchial hypersecretion. MATERIALS AND METHODS:Cross-sectional study which included 43 non-smoking asthmatic patients without bronchiectasis, 19 with bronchiectasis, and 24 without bronchial hypersecretion. All patients underwent the following: IS, spirometry, fractional exhaled nitric oxide, prick test, total immunoglobulin E (IgE), and blood albumin. Analysis of mucins was determined by ELISA and expression of TLR2 and TLR4 by flow cytometry. The level of asthma control was determined by the Asthma Control Test (ACT) questionnaire and quality of life was assessed by the reduced version of the Asthma Quality of Life Questionnaire (mini-AQLQ). RESULTS:Asthmatics with bronchial hypersecretion were significantly older (62.6 years vs 48.5 years; p=0.02); had greater severity (persistent severe asthma 94.7% vs 29.2%; p=0.000); a higher proportion of nasal polyposis (36.8% vs 8.3%; p=0.022); less control of asthma (73.7% vs 8.3%; p=0,000); a higher proportion of asthma with negative prick test (68.4% vs 16.6%; p=0.001), and lower levels of IgE (113.4 IU/mL vs 448 IU/mL; p=0.007), compared with asthmatics without bronchial hypersecretion. Significant differences were observed neither in the expression of TLRs 2 and 4 in inflammatory cells of IS or peripheral blood, nor in the expression of mucins between both groups. CONCLUSION:Asthma patients with bronchial hypersecretion have more severe and uncontrolled disease, with poor quality of life as well as a non-allergic inflammatory phenotype. Within the mechanisms involving these differences, it does not appear that mucins and TLRs play an important role.

Emerging data suggest that innate immunity may play a role in asthma, particularly the toll-like receptors (TLRs). Some studies pointed to an involvement of TLRs 2 and 4 in the pathogenesis of allergic asthma, and other studies related TLRs to IgE. However, there are not any studies that have comprehensively evaluated the expression of TLRs 2 and 4 in inflammatory cells, in peripheral blood and induced sputum specimens from asthmatic patients, according to their total serum IgE.

RATIONALE:Mucins are essential for airway defense against bacteria. We hypothesized that abnormal secreted airway mucin levels would be associated with bacterial colonization in patients with severe chronic obstructive pulmonary disease (COPD) Objectives: To investigate the relationship between mucin levels and the presence of potentially pathogenic micro-organisms in the airways of stable patients with severe COPD Methods: Clinically stable patients with severe COPD were examined prospectively. All patients underwent a computerized tomography scan, lung function tests, induced sputum collection, and bronchoscopy with bronchoalveolar lavage (BAL) and protected specimen brush. Patients with bronchiectasis were excluded. Secreted mucins (MUC2, MUC5AC, and MUC5B) and inflammatory markers were assessed in BAL and sputum by ELISA.MEASUREMENTS AND MAIN RESULTS:We enrolled 45 patients, with mean age (±SD) of 67 (±8) years and mean FEV1 of 41 (±10) % predicted. A total of 31% (n = 14) of patients had potentially pathogenic micro-organisms in quantitative bacterial cultures of samples obtained by protected specimen brush. Patients with COPD with positive cultures had lower levels of MUC2 both in BAL (P = 0.02) and in sputum (P = 0.01). No differences in MUC5B or MUC5AC levels were observed among the groups. Lower MUC2 levels were correlated with lower FEV1 (r = 0.32, P = 0.04) and higher sputum IL-6 (r = -0.40, P = 0.01).CONCLUSIONS:Airway MUC2 levels are decreased in patients with severe COPD colonized by potentially pathogenic micro-organisms. These findings may indicate one of the mechanisms underlying airway colonization in patients with severe COPD. Clinical trial registered with www.clinicaltrials.gov (NCT01976117).

Background: Measurement of the fractional exhaled nitric oxide (FeNO) and eosinophils in induced sputum are noninvasive markers for assessing airway inflammation in asthma. The clinical usefulness of the correlation between raised FeNO and sputum eosinophilia is controversial. We aimed to examine dissociation between FeNO and sputum eosinophils in a clinical series of asthma patients and to determine whether dissociation between these noninvasive markers was associated with clinical and inflammatory differences in these patients. Methods and findings: A total of 110 patients with asthma were included in a cross-sectional study. All of them were on maintenance treatment for asthma. All patients underwent the following on the same day: FeNO, induced sputum, spirometry, serum total IgE levels and skin prick test. The level of asthma control was determined by the Asthma control Test Questionnaire. In 46 (41.8%) patients, a discrepancy between FeNO and sputum eosinophil count was observed, of those, 34 (73.9%) had a FeNO <50ppb and high eosinophil count, and were characterized by having a predominance of nonallergic asthma with bronchial eosinophilic inflammatory phenotype. Also, 12 (26.1%) patients had FeNO 50ppb and sputum eosinophilia within the normal reference values, and were characterized by having a predominance of atopy with a paucigranulocytic inflammatory phenotype. Conclusions: A high percentage of patients with dissociation between results of FeNO and sputum eosinophils was observed. These patients showed differential clinical and inflammatory features.

Objective: To determine the general and specific utility in diagnosis and/or treatment of induced sputum (IS) inflammatory cell counts in routine clinical practice.Methods: Retrospective study of 171 patients referred for clinical sputum induction over a 1-year period in the pulmonology department of a referral hospital. Independent observers established whether the information provided by IS inflammatory cell count was useful for making diagnostic and therapeutic decisions.Results: The most frequent reasons for determination of IS inflammatory cell count were: asthma 103 (59.20%); uncontrolled asthma 34 (19.54%); chronic cough 19 (10.9%), and gastroesophageal reflux 15 (8.6%). In 115 patients (67.3%) it was generally useful for diagnosis and/or treatment; in 98 patients (57.3%) it provided diagnostic information and in 85 patients (49.7%) it assisted in therapeutic decision making. In asthma, uncontrolled asthma, chronic cough and gastroesophageal reflux, the results were useful in 71.8%, 67.6%, 47.4% and 60%, respectively.Conclusion: The information provided by IS inflammatory cell count is extremely useful in clinical practice, especially in asthma and chronic cough. These results may justify the inclusion of the IS technique in pulmonology departments and asthma units of referral centers. (C) 2015 SEPAR. Published by Elsevier Espana, S.L.U. All rights reserved.

Introduction: Recent studies have found variability in asthma inflammatory phenotypes determined by the inflammatory cells in induced sputum (IS). The aim of this study was to determine the frequency and factors affecting inflammatory phenotype variability in IS.Methods: Retrospective observational study that included 61 asthmatic patients who underwent at least two IS tests over a period of 5 years. They were classified according to their baseline inflammatory phenotype and subsequently grouped according to phenotype variability (persistent eosinophilic, persistent non-eosinophilic and intermittent eosinophilic). Demographic, clinical and functional data and factors potentially influencing IS variability were collected in all cases.Results: Of the 61 patients, 31 (50.8%) had a change with respect to baseline inflammatory phenotype. Of these, 16 (51.6%) were eosinophilic, 5 (16.1%) neutrophilic, 1 (3.2%) mixed and 9 (29.1%) paucigranulocytic. According to phenotype variability, 18 patients (29.5%) were classified as persistent eosinophilic, 17 (27.9%) non-persistent eosinophilic, and 26 (42.6%) intermittent eosinophilic. Smoking and recent asthma exacerbation were significantly associated with increased risk of variability of the IS inflammatory phenotype (OR = 6.44; p = .013; 95% CI = 1.49-27.80 and OR = 5.84; p = .022; 95% CI = 1.29-26.37, respectively).Conclusion: Half of asthma patients, predominantly those with eosinophilic phenotype, piesent a change in IS inflammatory phenotype. This variability is associated with smoking and recent asthma exacerbation. Data suggest these factors can modify the classification of IS inflammatory phenotype in clinical practice. (C) 2014 SEPAR. Published by Elsevier Espana, S.L.U. All rights reserved.

Hypersecretion bronchial asthma is a poorly characterized variant of asthmatic disease. Probably its pathogenesis is related with impaired innate immunity.

Background: Exhaled breath temperature (EBT) has recently been proposed as a noninvasive marker of bronchial inflammation in patients with asthma. However, the usefulness of EBT in everyday clinical practice is not well established. Results to date are contradictory and are mainly derived from small, pediatric populations. A comparison of results is further complicated by the use of different equipment and measurements. Objective: We performed a comprehensive study to determine whether EBT is related to asthma control, disease severity, bronchial obstruction, or bronchial inflammation. Methods: Sixty-nine patients on maintenance treatment for asthma were included in a cross-sectional study. At the same visit, we measured the EBT plateau (EBTp) using an X-halo Breath Thermometer (Delmedica, Singapore), the fraction of exhaled nitric oxide (FeNO), spirometry, and inflammatory cell count in induced sputum, and we administered the Asthma Control Test questionnaire. Results: No significant differences were found between EBTp measurements and the level of asthma control, disease severity, bronchial obstruction, FeNO levels, or inflammatory asthma phenotypes. We found a significant difference between EBTp and gender. The EBTp was 34.07°C (SD 0.74) in women and 34.38°C (0.46) in men (p = 0.038). We also found a significant correlation between EBTp measurements and the induced sputum eosinophil count (R = -0.348, p = 0.003). Conclusions: The results of this study do not support the usefulness of the EBTp in asthma management in routine clinical practice. Further research using standardized methods is needed to determine the potential use of the EBTp measurement in asthma management.

BACKGROUND AND OBJECTIVE Patients with persistent asthma have different inflammatory phenotypes. The electronic nose is a new technology capable of distinguishing volatile organic compound (VOC) breath-prints in exhaled breath. The aim of the study was to investigate the capacity of electronic nose breath-print analysis to discriminate between different inflammatory asthma phenotypes (eosinophilic, neutrophilic, paucigranulocytic) determined by induced sputum in patients with persistent asthma. METHODS Fifty-two patients with persistent asthma were consecutively included in a cross-sectional proof-of-concept study. Inflammatory asthma phenotypes (eosinophilic, neutrophilic and paucigranulocytic) were recognized by inflammatory cell counts in induced sputum. VOC breath-prints were analyzed using the electronic nose Cyranose 320 and assessed by discriminant analysis on principal component reduction, resulting in cross-validated accuracy values. Receiver operating characteristic (ROC) curves were calculated. RESULTS VOC breath-prints were different in eosinophilic asthmatics compared with both neutrophilic asthmatics (accuracy 73%; P=.008; area under ROC, 0.92) and paucigranulocytic asthmatics (accuracy 74%; P=.004; area under ROC, 0.79). Likewise, neutrophilic and paucigranulocytic breath-prints were also different (accuracy 89%; P=.001; area under ROC, 0.88). CONCLUSION An electronic nose can discriminate inflammatory phenotypes in patients with persistent asthma in a regular clinical setting. ClinicalTrials.gov identifier: NCT02026336.

Rationale: Mucins are mucus glycoproteins essential for airway protection. We hypothesized that lower airway mucins levels may affect bacterial colonization in stable patients with severe Chronic Obstructive Pulmonary Disease (COPD). Objective: To assess the association between secreted mucin levels and the presence of airway PPB in stable severe COPD patients. Material and methods: Clinically stable (g6 weeks) severe COPD patients were examined prospectively. All patients underwent a CT scan, sputum collection and bronchoscopy with bronchoalveolar lavage (BAL) and protected specimen brush (PSB). Patients with bronchiectasis or other lung diseases were excluded. Samples were processed for microbiological cultures and detection of secreted mucins (MUC2, MUC5AC and MUC5B) using ELISAs. Bacterial colonization was considered when PSB culture was positive for Potentially Pathogenic Bacteria (PPB). Results: We enrolled 45 COPD patients, with mean age (SD) of 67 (±8) years and mean FEV 1 of 41% (±10) of predicted. In 14/45 patients (31%), bronchoscopic samples were positive for PPB. H. influenzae was the most common PPB (57%). There were no differences in age, gender, lung function and COPD treatment among colonized and non-colonized patients. Colonized COPD patients had lower levels of MUC2 in BAL and sputum, with statistically significant differences in sputum (60 ±31 vs. 38 ±33 ng/dL, p=0.04). No differences in MUC5B and MUC5AC levels were observed among groups. Conclusions: Secreted airway MUC2 levels are decreased in severe COPD patients colonized by PPB. These findings may be one of the mechanisms that could explain the airway colonization of stable COPD patients. Funded by ISCIII (PS09/2567).

Recently it has involved the role of TLRs (toll-like receptors) in the pathogenesis of asthma.The possible role that TLRs play in IgE-dependent asthma (not eosinophilic) and its recognition as a new endotype asthma, could open new therapeutic expectations. Objective: To analyze the expression of TLR 2 and 4 in monocytes/ macrophages and neutrophils in peripheral blood and induced sputum from asthmatic patients IgE dependent (IgEdep) vs. IgE dependent (IgEnodep). Method : We studied 36 patients with asthma. Asthma ranked IgE dependent (n = 13) and non-dependent (n = 23) according to the level of IgE in the blood. All patients underwent the same day an induced sputum, pulmonary function studies, FeNO, blood total IgE and skin test by prick technique. The cellular composition was analyzed by flow cytometry. Expression of TLRs were analyzed using monoclonal antibodies conjugated with fluorochromes appropriate. Results: Descriptive analysis intergroup and between categorical variables was not significant. The percentage of neutrophils TLR4 + in induced sputum was 1.51% (± 2.98) for asthmatics IgEnodep and 11.17% (±25.15) for asthmatics IgEdep, with a statistically significant correlation (p = 0.006). No significant differences were found among the other groups. Conclusion : The percentage of neutrophils expressing TLR4 in induced sputum decreases in asthma not eosinophilic. This could suggest that in this type of asthma the defense mechanism of neutrophils could be altered by decreasing expression of these receptors on their cell surface. This mechanism would still be defined. Probably the respiratory infections play an important role.

Identifying the inflammatory phenotype of asthmatic patients requires a time-consuming methodology, personnel and technical resources. The electronic nose is a device capable of detecting volatile organic compounds (VOCs) present in the gas phase of human respiration. Objectives : To compare the profiles of VOCs in the air exhaled by the electronic nose with bronchial inflammatory phenotypes of asthma who attend outpatient. Methods: A total of 44 asthmatic patients were included (16 with asthma, 8 with neutrophilic asthma and 20 with paucigranulocytic asthma). All patients underwent the same day of the visit an: induced sputum, pulmonary function studies and fractional exhaled nitric oxide. Asthmatic patients were classified as induced sputum cellularity (inflammatory profile). The determination of VOCs in the exhaled air is conducted through an electronic nose Cyranose 320 (Smith Detections, Pasadena, CA) according to the method described by Dragonieri S, et al. The breathprints produced by the electronic nose is mathematically analyzed by logarithmic regression, represented unilaterally and bidimensional for further analysis and interpretation. Results : Descriptive analysis intergroup and between categorical variables was not significant.The electronic nose was able to discriminate correctly by 100% to asthmatic vs. neutrophilic and vs paucigranulocytic asthma and 90% recall rate when comparing neutrophilic vs paucigranulocytic Conclusion: The results indicate that the electronic nose is a noninvasive method that allows discriminate the different inflammatory phenotypes of asthma especially those with a eosinophilic asthma.