As part of our ongoing mission to expand horizons in spondyloarthritis research, the Spondylitis Association of America hopes to encourage new, upcoming rheumatologists and researchers to focus on the future of treatment and research in ankylosing spondylitis and related diseases.
To this end, we created the Spondylitis Association of America/Bruckel Early Career Investigator Award, which recognizes outstanding "contributions to the care and understanding of patients with spondyloarthritis." The award winner receives a $20,000 grant from SAA for use in spondyloarthritis research. The award, named in honor of our co-founder Jane Bruckel, is given annually to the early career investigator who shows the most promise to contribute to the understanding or therapy of axial spondyloarthritis.
Joerg Ermann is a rheumatologist at Brigham and Women’s Hospital (BWH) and Instructor at Harvard Medical School with a research background in cellular/molecular immunology and animal models of autoimmune disease.
Dr. Ermann’s interest in ankylosing spondylitis and spondyloarthritis (AS/SpA) was sparked by patient encounters early during a rheumatology fellowship. As a doctor with significant understanding of musculoskeletal disease and systemic autoimmune conditions, he recognized the unmet need for further research. Dr. Ermann then chose to focus his research on AS/SpA disease mechanisms with the goal of using relevant mouse models and translational research approaches to understand AS/SpA pathogenesis with the ultimate goal of developing better therapies.
About Dr. Ermann’s Award-Winning Work
Dr. Ermann’s research focuses on the overlap between the genetic factors and disease mechanisms driving As/SpA and inflammatory bowel disease (IBD). Using the aforementioned mouse models that strongly resemble human conditions, specifically TRUC (T-bet-/- Rag2-/- Ulcerative Colitis), he was able to identify a number of cytokines (small proteins that affect intercellular communication and interaction), Il-17A, Il-23 and Il-1, that are critical in the pathogenesis of AS/SpA. This discovery will enable him to research the mechanisms of pathological new bone formation as a result of these cytokine interactions.
Jessica Walsh, MD, is a rheumatologist and Assistant Professor at the University of Utah School of Medicine, Division of Rheumatology who has dedicated her career to spondyloarthritis patients.
Dr. Walsh received her B.A. in Biology from Whitman College in Washington. She then moved to Utah where she spent the next 16 years advancing her career in Rheumatology. In 2003 she received her MD from the University of Utah School of Medicine and proceeded to obtain her Intern, Resident, Chief Resident and Fellow statuses before finally receiving her M.S.C.I. in 2015. Over her distinguished career, she has achieved numerous board certifications and scholastic honors, published many peer-reviewed journal articles/abstracts, and has presented 7 oral presentations to various institutions and associations. Her clinical practice is dedicated to those affected by spondyloarthritis, hosting four half-day SpA clinics per week with the primary goal of improving early disease recognition.
Dr. Walsh is a strong believer that high quality observational data is critical for understanding SpA and her work in registry has allowed the development of powerful methodologies for SpA research in large datasets. To date, she has enrolled over 652 participants in registries at the University of Utah and the Salt Lake City Veterans Affair (VA) Medical Center and has designed many others such as the Utah Psoriasis Initiative Arthritis (UPI Arthritis), Psoriatic Arthritis Research Collaboration (PARC), Longterm Outcomes with B27 And Spondyloarthritis (LOBAS), and the Program to Understand the Longterm Outcomes of SpondyloARthritis (PULSAR). In addition to registry work, she has conducted extensive research in Veterans Affair databases and collaborated with bioinformatics experts to develop previously unfeasible methods of identifying undiagnosed individuals. Her registry and database research has contributed to our scientific knowledge in the areas of screening instruments, severity measurement tools, work disability, gender differences, perceptions of therapy, fatigue, sleep apnea, and other comorbidities.
Mark Asquith is a research assistant professor at the Oregon Health & Science University with a specialization in microbiome studies.
Dr. Asquith received his BSc in Biology from the University of Nottingham in 2004. While acquiring his PhD from Oxford University (2009), he was trained by Fiona Powrie, arguably one of the leading immunologists in the world. Since then, he has undertaken multiple fellowships and written numerous publications that have contributed to the understanding of arthritis and spondyloarthritis – some of which have been selected for oral presentation at the American College of Rheumatology. His scientific career has been dedicated to the identification and functional characterization of inflammatory and regulatory immune mechanisms in rheumatic disease.
For over a decade, Dr. Asquith has been actively researching the intricate relationship between the immune system and the trillions of microbes that inhabit the intestinal tract, the latter commonly known as the gut microbiome. His previous studies have made it increasingly clear that the impact of the intestinal microbiome extends far beyond the gut, affecting conditions as diverse as autism, diabetes, arthritis and spondyloarthritis. The current focus of his laboratory has thus been to provide a novel diagnostic for spondyloarthritis as well as determine therapeutic targets for its clinical management. To accomplish this, studies are being performed on the intestinal microbiome and immune functions in both SpA patient populations and the HLA-B27 transgenic rat in order to identify potent changes to the microbial and metabolite constitution in SpA and bridge the gap between phenotypical and pathophysiological pathways.
Pamela Weiss, MD, MSCE, is a pediatric rheumatologist at Children’s Hospital of Philadelphia (CHOP) whose clinical and research interests are focused on juvenile spondyloarthritis (JSpA).
Dr. Weiss earned an A.B. in Molecular Biology from Princeton University, and her medical degree from Albert Einstein College of Medicine (2002). She completed both her Pediatrics Residency and Rheumatology fellowship training at CHOP. Dr. Weiss was co-principal investigator of the American College of Rheumatology (ACR) JIA Treatment Recommendations Update, as well as a member of the Core Expert Panel for development of the 2014 Clinical Practice Guidelines for Axial Spondyloarthritis, a collaborative undertaking between ACR, SAA, and SPARTAN. Additionally, Dr. Weiss serves on the ACR Pediatric Rheumatology Special Committee. Her commitment to research and improving the care of children with juvenile arthritis is also evident in her roles as vice chair of the Childhood Arthritis & Rheumatology Research Alliance (CARRA) Juvenile Arthritis Research Committee and her recent appointment as Clinical Research Director for the CHOP Division of Rheumatology. She has lectured nationally and internationally on juvenile arthritis and spondyloarthritis.
Dr. Weiss’ research focuses on the pharmacoepidemiology and outcomes of JSpA. JSpA is an umbrella term that also encompasses three categories of juvenile idiopathic arthritis (JIA) -- enthesitis-related arthritis (ERA), juvenile psoriatic arthritis, and undifferentiated arthritis (children who meet criteria for more than one JIA category). Using patient-reported data from the CHOP clinic, she demonstrated that children with ERA have worse function, poorer quality of life, and higher pain intensity than children with other categories of JIA. She confirmed and published these findings using a large national registry of pediatric rheumatic diseases. To address the knowledge gaps of this understudied condition, her efforts are specifically directed to better defining the disease and developing treatment strategies for children that will directly improve both clinical and patient-reported outcomes.
Nigil Haroon, MD, PhD, is a rheumatologist at the University Health Network and an assistant professor of medicine and rheumatology at the University of Toronto. He has a keen interest in ankylosing spondylitis (AS). Specifically, his area of research includes radiographic progression, identifying novel therapeutic targets and understanding the immunology and genetics of AS. He is well published in this area and has been an invited speaker at several international meetings. Dr. Haroon has won several awards, including a CRA young faculty award for both clinical and basic research and, in 2013, the Spondylitis Association of America/Bruckel Early Career Investigator Award.
Dr. Haroon has a well-established translational research program at the University Health Network in Toronto and is renowned for his work in the functional genomics of AS, especially the role of a new gene, ERAP1, which was found to be strongly associated with AS in genome-wide association studies. He has published paradigm-shifting studies in AS, including work on disease modification in AS with tumor necrosis factor (TNF) inhibitors. He published the largest population based study in AS, showing a significantly increased risk of mortality in AS patients after experiencing heart attacks and strokes. As a result of this study, there is now an emphasis on early identification and treatment of traditional cardiovascular risk factors in AS patients.
Lianne Gensler, MD, is a rheumatologist at the University of California, San Francisco (UCSF) Medical Center and is director of the Ankylosing Spondylitis Clinic.
Dr. Gensler earned a medical degree at the University of California, Irvine. She completed an internal medicine residency, chief residency, and rheumatology fellowship at UCSF and then joined the medical staff in rheumatology. Her primary research interest is in studying the disease progression of ankylosing spondylitis and identifying predictors of osteoporosis development in patients with systemic lupus erythematosus. She is an assistant clinical professor of medicine at UCSF.
Dr. Gensler states, “Though we believe that ankylosing spondylitis is strongly rooted in genetics, what we are less clear on is how we can slow down its progression. Through our research, we have been able to show that smoking is a risk for progression, doubling the odds. We have also shown for the first time that patients who use the biologic agents - (TNF inhibitors) - have a more than 50 percent reduction in the risk of progression. It is not clear that everyone needs these drugs, as some patients may never progress, and some patients may be able to mitigate this progression by other modalities. I am thrilled to be able to continue to work on these ideas and help move the field forward.”
Judith Anne Smith, MD, graduated summa cum laude from Yale University. She then completed her MD/PhD program at the University of Chicago NIH Medical Scientist Training Program. Her graduate work in immunology was performed under the guidance of Dr. Jeffrey Bluestone. After completing her medical degree, she completed her pediatrics residency and pediatric rheumatology fellowship training at Cincinnati Children’s Hospital. Her fellowship training, under Dr. Robert Colbert, inspired her to pursue research in the pathogenesis of ankylosing spondylitis (AS) and related conditions. She joined the faculty as an assistant professor in pediatrics at the University of Wisconsin in Madison, where she continues to care for pediatric patients in the Pediatric Rheumatology Clinic and leads an active research program. Dr. Smith’s research goal remains to elucidate the fundamental processes that drive the evolution of ankylosing spondylitis in hopes of ultimately leading to more rational therapeutic development.
The macrophage is an important cell in the inflammatory response. Macrophages and other cells in the immune system produce cytokines such as tumor necrosis factor (TNF) when they are activated. Inhibition of these cytokines can be an effective therapeutic strategy in AS.
Dr. Smith and her colleagues at the University of Wisconsin showed that, compared to healthy controls, macrophages from patients with ankylosing spondylitis make more cytokines when stimulated with a bacterial product. The cytokine, IL-23, was especially increased. Pharmaceutical companies are actively testing inhibitors of IL-23 or inhibitors that target cytokines induced by IL-23 as potential treatment for AS.
For more than 30 years, the Spondylitis Association of America has spoken out on behalf of all who suffer from spondylitis. By making a donation to SAA, you will directly contribute to much-needed public awareness efforts, educational outreach programs, research initiatives, treatment advances and the ongoing search for the cure. Add your voice to our mission to be a leader in the quest to cure ankylosing spondylitis and related diseases, and to empower those affected to live life to the fullest. Together, our voice is louder. Together, we make a difference.
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