Stefano Guerra

Stefano Guerra

Director, Epidemiology
Professor, Public Health
Professor, Medicine - (Tenure Track)
Research Scientist, Respiratory Sciences
Professor, BIO5 Institute
Contact
(520) 626-7411

Work Summary

Stefano Guerra's work includes an epidemiologic study, which used a household-based approach to assess prevalence and longitudinal changes in respiratory health. Other biomarker projects include a study on molecular biomarkers of asthma and COPD from the European Community Respiratory Health Survey.

Research Interest

Stefano Guerra, MD, PhD, is a professor of Medicine, the Director of the Population Science Unit at the Asthma and Airway Disease Research Center, and a leading expert in the natural history and biomarkers of obstructive lung diseases, including asthma and chronic obstructive pulmonary disease (COPD). As principal investigator, he is engaged in the leadership and coordination of multiple studies that use bio-specimens and phenotypic information from independent epidemiological cohorts to characterize the natural history, profile the risk factors, and identify novel biomarkers of lung diseases.

Publications

Lombardi, E., Stern, D., Sherrill, D., Morgan, W., Wright, A., Garcia-Aymerich, J., Serra Pons, I., Guerra, S., & Martinez, F. (2017). Peak flow variability in childhood and body mass index in adult life. Journal of Allergy and Clinical Immunology.
Vasquez, M. M., Hu, C., Roe, D. J., Halonen, M., & Guerra, S. (2017). Measurement error correction in the least absolute shrinkage and selection operator model when validation data are available. Statistical methods in medical research, 962280217734241.
BIO5 Collaborators
Stefano Guerra, Chengcheng Hu

Measurement of serum biomarkers by multiplex assays may be more variable as compared to single biomarker assays. Measurement error in these data may bias parameter estimates in regression analysis, which could mask true associations of serum biomarkers with an outcome. The Least Absolute Shrinkage and Selection Operator (LASSO) can be used for variable selection in these high-dimensional data. Furthermore, when the distribution of measurement error is assumed to be known or estimated with replication data, a simple measurement error correction method can be applied to the LASSO method. However, in practice the distribution of the measurement error is unknown and is expensive to estimate through replication both in monetary cost and need for greater amount of sample which is often limited in quantity. We adapt an existing bias correction approach by estimating the measurement error using validation data in which a subset of serum biomarkers are re-measured on a random subset of the study sample. We evaluate this method using simulated data and data from the Tucson Epidemiological Study of Airway Obstructive Disease (TESAOD). We show that the bias in parameter estimation is reduced and variable selection is improved.

Xu, C., others, ., Guerra, S., others, ., & Koppelman, G. (2017). Epigenome-wide meta-analysis identifies reduced DNA methylation reflecting eosinophil and T cell gene expression signatures in childhood asthma. Lancet Resp Med.
Vasquez, M., Sherill, D., LeVan, T., Morgan, W., Sisson, J., & Guerra, S. (2017). Persistent light to moderate alcohol intake and lung function: a longitudinal study. Alcohol.
Bousquet, J., Anto, J. M., Wickman, M., Keil, T., Valenta, R., Haahtela, T., Lodrup Carlsen, K., van Hage, M., Akdis, C., Bachert, C., Akdis, M., Auffray, C., Annesi-Maesano, I., Bindslev-Jensen, C., Cambon-Thomsen, A., Carlsen, K. H., Chatzi, L., Forastiere, F., Garcia-Aymerich, J., , Gehrig, U., et al. (2015). Are allergic multimorbidities and IgE polysensitization associated with the persistence or re-occurrence of foetal type 2 signalling? The MeDALL hypothesis. Allergy, 70(9), 1062-78.

Allergic diseases [asthma, rhinitis and atopic dermatitis (AD)] are complex. They are associated with allergen-specific IgE and nonallergic mechanisms that may coexist in the same patient. In addition, these diseases tend to cluster and patients present concomitant or consecutive diseases (multimorbidity). IgE sensitization should be considered as a quantitative trait. Important clinical and immunological differences exist between mono- and polysensitized subjects. Multimorbidities of allergic diseases share common causal mechanisms that are only partly IgE-mediated. Persistence of allergic diseases over time is associated with multimorbidity and/or IgE polysensitization. The importance of the family history of allergy may decrease with age. This review puts forward the hypothesis that allergic multimorbidities and IgE polysensitization are associated and related to the persistence or re-occurrence of foetal type 2 signalling. Asthma, rhinitis and AD are manifestations of a common systemic immune imbalance (mesodermal origin) with specific patterns of remodelling (ectodermal or endodermal origin). This study proposes a new classification of IgE-mediated allergic diseases that allows the definition of novel phenotypes to (i) better understand genetic and epigenetic mechanisms, (ii) better stratify allergic preschool children for prognosis and (iii) propose novel strategies of treatment and prevention.