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Asthma and allergic diseases are a serious public health burden and affect over 40% of the population worldwide. In the Division of Asthma Research our overarching goal is to develop new prevention and treatment strategies for allergic diseases that are personalized and target high risk populations at the critical time periods when they are most vulnerable.
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In the Division of Asthma Research we are focused on understanding the total exposure relevant to asthma from the cell and individual level to the patient, family neighborhood and community level. We aim to identify the factors that contribute to asthma development and symptoms, determine the mechanisms by which these factors contribute to disease, delineate how effects of environmental exposure are modified by genetics and other exposures, and identify biomarkers of exposure and disease activity and severity in an individual. Our current projects include a spectrum of basic, translational and clinical research that investigates the role of these factor in promoting disease development and activity.
The division utilizes transdisciplinary approaches integrating human cohorts, in vitro systems, and animal models to address these complex problems. Numerous other factors affect disease outcomes as well including psychosocial factors, community health perceptions, and health literacy.
is proxy for secondhand smoke (SHS) exposure.
Genetic variation along nicotine and cotinine metabolic pathways may
alter the internal cotinine close, leading to misinterpretations of exposure
health outcomes association. Caucasian
children with available SHS exposure and hair cotinine data were genotyped for
Reprinted from Fig. 3 published in J Allergy Clin Immunol 2014 May 13. Showing
hypothesized shared pathways leading to asthma and inflammation. Copyright © 2014, Biagini Myers
et al. with permissions from Elsevier.
Asthma is the most common chronic illness
in children in the U.S. Epithelial genes have previously been associated with
asthma but, only explain a small fraction of heritability. In part, this might
be due to epistasis, which is often not considered. In this study we sought to determine
independent and epistatic associations between FLG, SPINK5 and TSLP gene
variants and childhood asthma.
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