News Release

Genetic link found between spinal arthritis and inflammatory bowel disease

Peer-Reviewed Publication

PLOS

Researchers at the University of Queensland Diamantina Institute in Brisbane, Australia, have found that a form of spinal arthritis is genetically linked to Inflammatory Bowel Disease. The study will be published on December 2 in the open-access journal PLoS Genetics. Ankylosing Spondylitis (AS) is a common form of arthritis involving chronic inflammation particularly of the spinal and pelvic joints, which causes pain, stiffness, and often disability. Affecting up to 0.5% of the population, the risk of AS is almost entirely genetically determined. Curiously, AS patients appear to be highly susceptible to Inflammatory Bowel Disease (IBD), including Crohn's disease. Similarly, the development of AS is common in IBD patients. Professor Matt Brown and his colleagues wanted to determine if this was more than a coincidence.

"It seemed likely that common pathogenic pathways may be acting in the development of both diseases" said Professor Brown.

In order to test whether genes associated with Crohn's disease are also associated with AS, they searched for known genetic markers of Crohn's disease in the genomes of more than 2700 AS patients, working with colleagues from England, North America and Canada. The results revealed that both AS and Crohn's disease share several similar genetic variations, and identified seven genes affecting both conditions.

When the researchers took a closer look at the function of the genes they had identified, they found that four of the genes are known to influence the activation of a recently discovered class of helper T-cells called Th17 cells. Identifying the involvement of these immune cells greatly increases what is known about how AS develops, and points to potential new therapies for this form of arthritis. This study highlights the value of studies that look into individual genes that might be implicated in related diseases.

###

FINANCIAL DISCLOSURE: This study was funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) grants P01-052915 and R01-AR046208. Funding was also received from the University of Texas at Houston CTSA grant UL1RR024188, Cedars-Sinai GCRC grant MO1-RR00425, Intramural Research Program, NIAMS/NIH, and Rebecca Cooper Foundation (Australia). MAB is funded by the National Health and Medical Research Council (Australia). Support was also received from the National Institute for Health Research (UK) Oxford Biomedical Research Centre ankylosing spondylitis chronic disease cohort (Theme Code A91202), NIHR Oxford Musculoskeletal Biomedical Research Unit and the NIHR Thames Valley Collaborative Local Research Network, and Princess Alexandra Hospital Research Foundation. We would like to thank the National Ankylosing Spondylitis Society (UK) for assistance in patient recruitment and the Arthritis Research Campaign (UK) for financial support under grants 19356 and 18797. The Spondyloarthritis Research Consortium of Canada (SPARCC) is supported by a National Research Initiative (NRI) award from the Arthritis Society of Canada. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

COMPETING INTERESTS: The authors have declared that no competing interests exist.

CITATION: Danoy P, Pryce K, Hadler J, Bradbury LA, Farrar C, et al. (2010) Association of Variants at 1q32 and STAT3 with Ankylosing Spondylitis Suggests Genetic Overlap with Crohn's Disease. PLoS Genet 6(12): e1001195. doi:10.1371/journal.pgen.1001195

PLEASE ADD THIS LINK TO THE FREELY AVAILABLE ARTICLE IN ONLINE VERSIONS OF YOUR REPORT (the link will go live when the embargo ends): http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1001195

PRESS-ONLY PREVIEW OF THE ARTICLE: http://www.plos.org/press/plge-06-12-brown.pdf

CONTACT: Dr Fiona McMillan
Science Writer
University of Queensland Diamantina Institute
f.mcmillan@uq.edu.au
Tel: + 61 7 3176 6943

Disclaimer

This press release refers to an upcoming article in PLoS Genetics. The release is provided by journal staff, or by the article authors and/or their institutions. Any opinions expressed in this release or article are the personal views of the journal staff and/or article contributors, and do not necessarily represent the views or policies of PLoS. PLoS expressly disclaims any and all warranties and liability in connection with the information found in the releases and articles and your use of such information.

About PLoS Genetics

PLoS Genetics (http://www.plosgenetics.org) reflects the full breadth and interdisciplinary nature of genetics and genomics research by publishing outstanding original contributions in all areas of biology. All works published in PLoS Genetics are open access. Everything is immediately and freely available online throughout the world subject only to the condition that the original authorship and source are properly attributed. Copyright is retained by the authors. The Public Library of Science uses the Creative Commons Attribution License.

About the Public Library of Science

The Public Library of Science (PLoS) is a non-profit organization of scientists and physicians committed to making the world's scientific and medical literature a freely available public resource. For more information, visit http://www.plos.org.


Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.