Kelly Brown: Associate Professor at Department of Pediatrics, UBC Faculty of Medicine

Prospective Graduate Students / Postdocs

This faculty member is currently not looking for graduate students or Postdoctoral Fellows. Please do not contact the faculty member with any such requests.

Associate Professor

Faculty of Medicine

Research Classification

Medical, health and life sciences

Research Interests

childhood rheumatic diseases

Inflammation

phagocytes

Relevant Thesis-Based Degree Programs

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Affiliations to Research Centres, Institutes & Clusters

BC Children's Hospital Research Institute

Research Options

I am available and interested in collaborations (e.g. clusters, grants).

I am interested in and conduct interdisciplinary research.

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Biography

In Canada, rheumatic conditions are the most common chronic illness of childhood, affecting as many as 10 000 of our children and youth. Examples of rheumatic diseases are juvenile idiopathic arthritis, lupus, vasculitis and autoinflammatory conditions. The common denominator for all is pain and / or inflammation in joints, muscles, and critical organs. Some diseases are life- or organ- threatening and all have significant potential for lifelong poor health and disability. There are no cures and remarkably few treatments that are specific and safe for a growing child. My research program is designed to generate an evidence base for clinical decisions that ultimately improve outcomes for Canadian children and families affected by rheumatic disease.

Graduate Student Supervision

Master's Student Supervision

Theses completed in 2010 or later are listed below. Please note that there is a 6-12 month delay to add the latest theses.

Platelet factor 4 (PF4), a potential biomarker for disease activity in juvenile idiopathic arthritis (JIA) (2022)

Juvenile idiopathic arthritis (JIA) is the most common cause of youth disability in Canada, characterized by chronic joint inflammation and bone degradation. Common JIA treatment regimens include nonsteroidal anti-inflammatory drugs (NSAIDs), and disease-modifying agents. Currently, there are no reliable means to identify those children with JIA at risk of a more severe or progressive or frequently relapsing disease. Platelets are blood cells with well characterized roles in hemostasis and increasingly recognized contributions to inflammation in chronic inflammatory disease. Specifically, the presence of platelet factor 4 (the most abundant platelet-derived chemokine) and activated platelets have been associated with inflammation in rheumatoid joints in adults. However, the role of platelet-derived proteins in juvenile arthritis has not yet been evaluated. This patient-based study evaluated platelet factor 4 (PF4) as a potential subclinical marker of disease activity in JIA and explored a possible cross-talk with neutrophils and neutrophil-derived S100A proteins (S100A8/9 and S100A12) that have been shown to track with JIA disease activity. Results demonstrated that intracellular (within platelets) and extracellular (in plasma) PF4 was significantly more abundant in healthy children compared to adults, and release of PF4 from thrombin receptor-activated platelets was enhanced with prior exposure to S100A12 and S100A8/9. In contrast, PF4 did not stimulate pro-inflammatory responses (release of reactive oxygen species or S100A protein) by neutrophils. Early in JIA disease course and in the absence of NSAID treatment, there was a moderate correlation between circulating concentrations of PF4 and both disease activity and concentrations of S100A12. For patients in remission, circulating PF4 concentrations were higher in children who relapsed, correlated with the time to first flare, and had a similar probability of predicting a flare compared to S100A12. Overall, this study helped to advance our understanding of the role of platelets in chronic inflammation and provided preliminary evidence for PF4 as a subclinical marker for JIA disease activity.

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