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Spondylitis Association of America Research Article Archive

Health research has high value to society. It can provide important information about disease trends and risk factors, outcomes of treatment, functional abilities, patterns of care, and health care costs and use. The different approaches to research provide complementary insights. Clinical trials can provide important information about the efficacy and adverse effects of medical interventions by controlling the variables that could impact the results of the study, but feedback from real-world clinical experience is also crucial for comparing and improving the use of drugs, vaccines, medical devices, and diagnostics.

Below you will find links to some of the studies that have contributed to our increased understanding of spondyloarthritis.

SAA receives no government funding and relies on the generous donations from individuals to create and maintain the programs and services aimed at improving the futures of the 2.7 million Americans affected by spondylitis.

Research Article Archive

The Transition of Acute to Chronic Bowel Inflammation in Spondyloarthritis

Liesbet Van Praet, Peggy Jacques, Filip Van den Bosch and Dirk Elewaut

Abstract

That gut and joint inflammation are linked in spondyloarthritis (SpA) has been recognized for almost three decades. Intriguingly, microscopic gut inflammation, which occurs frequently in patients with SpA, is an important risk factor for clinically overt Crohn’s disease and ankylosing spondylitis. This Review describes current insights into the underlying mechanisms that lead to chronic gut inflammation in patients with SpA. We propose that the development of chronic bowel inflammation in these individuals occurs through a transition phase, in which inflammation evolves from an acute into a chronic state. Our transition model implies that different cell types are involved at different stages during disease progression, with stromal cells having an important role in chronicity. In addition, deficient regulatory feedback mechanisms or genetically determined alterations in antigen presentation, endoplasmic reticulum stress, autophagy or cytokine signaling might also favor a transition from self-limiting acute inflammation to chronic inflammation. We anticipate that this transition phase might be an important window for therapeutic intervention.

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