Dr Candice Quin

Research Overview

Dr. Quin aims to prevent the pathogenesis of frailty in older adults, providing them with more years of healthy, independent living. Frailty is a state of increased vulnerability to stressors including infections (e.g. pneumonia) and inflammatory diseases (e.g. cardiovascular disease, myelodysplastic syndrome [MDS], diabetes), which develops as a consequence of age-related decline in multiple systems, including the immune system. Using techniques such as flow cytometry, multi-omic approaches and gnotobiotics, Dr. Quin studies mechanisms by which gut microbiota shape the immune and epigenetic landscape to affect the development of frailty and ageing health conditions.

Find out more: https://www.quinlab.co.uk/lab/

Current Research

Major projects in the Quin lab include:

• Understanding the origins of healthy and unhealthy ageing (e.g. frailty) 
• Uncovering how the ageing gut microbiome contributes to age-related immune remodeling 
• Elucidating how changes in the gut microbiome impact host epigenomics
• Developing novel strategies to prevent age-related conditions (pneumonia, blood cancers, cardiovascular disease)

Past Research

Throughout my academic career, I have been fascinated with factors contributing to health across the life-course. I completed my Ph.D. in Biochemistry and Molecular Biology at the University of British Columbia under the supervision of Dr. Deanna Gibson. My doctoral training focused on how neonatal environmental exposures, such as diet, set up the ageing trajectory and alter systemic inflammation into adulthood through gut-microbe interactions. Here, I gained valuable insights into how different fat types (saturated, monounsaturated etc.) contribute to inflammation directly and through the microbiome. I then joined Dr. Dawn Bowdish’s research group at McMaster University as a postdoctoral researcher. In this position, I addressed important topics in immunology including the impact of the ageing microenvironment on haematopoiesis and epigenetic reprogramming of monocytes, the cellular and molecular mechanisms of impaired anti-pneumococcal immunity with age, and the role of inflammation in immunosenescence.