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Many patients with inflammatory bowel disease, rheumatoid arthritis, and ankylosing spondylitis also develop anaemia, which may impair their ability to exercise and perform normal activities. The cause of this anaemia is complex but is partly attributable to the effects of inflammatory molecules (cytokines) on the bone marrow, which produces new blood cells.
In work recently published in the Journal of Experimental Medicine, a team of researchers from the Kennedy Institute of Rheumatology led by Dr Thibault Griseri, shows that the cytokine interleukin-33 (IL-33) suppresses the production of new red blood cells in an experimental model of inflammatory arthritis and in human cells. This novel effect is caused by a direct effect of IL-33 to inhibit differentiation of red blood cell progenitors into mature cells.
"We are delighted to be able to share our work investigating a new pathway causing anaemia during inflammation. Anaemia is a common problem in patients with inflammatory diseases and we believe this work opens up a new area for development of possible therapies", said James Swann, DPhil student and first author of the paper.
This work identifies a new potential target for treatment of anaemia occurring as a comorbidity in patients with chronic inflammatory diseases.
The study was funded by Versus Arthritis, the Kennedy Trust for Rheumatology Research and the Wellcome Trust, and was a collaboration between the Griseri Lab and the Sansom Group at the Kennedy Institute.
