Around 40% of the world's population is now impacted by allergic disease and this figure
continues to rise. It is now understood that allergic disease arises from complex
interactions between genetic and environmental factors. Exposure to allergens such as dust
mites and pollen, as well as air pollutants such as diesel exhaust particulates, can alter
the ability of critical genes to be expressed appropriately, a process known as epigenetic
modification. The epigenetic modifications induced by allergens and pollutants appears to be
reversible, thus providing a mechanism by which allergic disease can be treated. Budesonide
(RhinocortĀ®) is a corticosteroid nasal spray commonly used to treat allergy symptoms. While
the anti- inflammatory and other pharmacological aspects of budesonide are well understood,
recent studies have suggested that budesonide may also work by reversing the epigenetic
modifications caused by allergen exposure, although this has not been examined in the context
of real-world exposures in humans.
This study aims to harness the power of epigenetic analysis to determine whether the
epigenetic landscape in patients suffering from allergic disease can be modified by the
administration of budesonide. It will fill critical gaps in understanding of epigenetic
effects and provide information to examine the connection between environmental impacts and
treatment effects. The research will expand the mechanistic understanding of the therapeutic
effects of budesonide for relief of nasal rhinitis symptoms and may reveal new mechanisms
that could improve treatment of allergies or pollution exposure, or serve as a tool for
evaluating future therapies. If this venture is successful, it will serve as a model for
studying and optimizing the epigenetic effects of other treatments and other diseases.
Phase:
Phase 4
Details
Lead Sponsor:
University of British Columbia
Collaborators:
Genome British Columbia Johnson & Johnson Consumer Inc. (J&JCI)