Anto J M

Biography

Since my training as specialist in Pneumology, most of my research has focused on the epidemiology of asthma and COPD. Contributions from studies I have led or co-led include: soybean epidemic asthma (Anto JM et al. Lancet 1986; Sunyer J et al. Lancet 1989; Anto JM et al. NEMJ 1989 & 1993); occupational asthma in the general population in Europe (Kogevinas M et al. Lancet 1999 & 2007); identification of major risk factors of adult asthma including exposure to cleaning products (Medina M et al. Thorax 2006; Zock JP et al. AJRCCM 2007); impact on respiratory health of unusual occupational and environmental episodes (Moya et al. Lancet 1994 ; Zock JP et al. AJRCCM 2007; Rodriguez-Trigo G et al. Ann Intern Med 2010); understanding of quality of life in COPD (Ferrer M et al. Ann Int Med 1997; Domingo A et al. AJRCCM 2002); lack of physical activity as risk factors of COPD exacerbations, COPD mortality, lung function decline and incidence of COPD (Garcia-Aymerich J et al. AJRCCM 2007). During the last years most of my research on asthma has been focused on the investigation on of the aetiology of asthma in the European Community Respiratory Survey (member of the Steering Committee; PI of the study in Spain). Based on the International Laboratory on Respiratory Epidemiology established by INSERM and CREAL (directors Francine Kauffmann and JM Antó) we have developed the MeDALL study (PIs: Jean Bousquet and Josep M. Antó; 12 M€; 21 partners; 2010-2015). MeDALL aims to generate novel knowledge on the mechanisms of initiation of allergy from early childhood to young adulthood (Bousquet J et al. Allergy 2011; Anto JM et al. JACI 2012).The main findings of my research have shown the importance of multimorbidity of asthma, rhinitis and eczema applying both canonical epidemiological methods (Pinart M et al. Lancet Resp Med 2014) and using a machine learning approach (Garcia-Aymerich J et al. Allergy 2015). To better understand the multimorbidity of these diseases we have developed an in silico model based on a computational analysis of the topology of the protein interaction network (Aguilar et al. Submitted). Our recent research on COPD has contributed to a new paradigm, that COPD is a heterogeneous entity witch clinical profiling involves the need of considering multiple traits including quality of life and exercise capacity in addition to lung function. We launched “The investigation of the phenotypic heterogeneity and course of COPD study” (Co-PI J Garcia-Aymerich). An unsupervised analysis of COPD patients revealed meaningful heterogeneity with one of the groups showing strong features of metabolic syndrome (Garcia-Aymerich J et al. Thorax 2011). The study established a simplified score for prediction of mortality in COPD (Puhan M et al. Lancet 2009). In a previous retrospective study we were among the first to show that COPD can start in early life (Svanes C et al. Thorax 2010); MeDALL has also contribute to understand the early life origins of COPD by showing that low concentrations of CC16 in serum are associated with reduced lung function in childhood, accelerated lung function decline in adulthood, and development of moderate airflow limitation in the general adult population (Guerra S et al Lancet Resp Med 2015).
Currently, my main scientific interest is to develop systems approach to respiratory diseases by applying new epidemiological methods to the understanding of multimorbidity (Antó JM et al. JACI 2016, Bousquet J & Anto JM et al. Allergy 2016).