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Rheumatoid Arthritis, Inflammation and a Hint of Watermelon

Molecule that gives watermelon its characteristic taste attached to peptides involved in triggering Rheumatoid Arthritis inflammation

By
Valerie Brown, Contributor
Saturday, May 27, 2017

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Rheumatoid arthritis (RA) is the second most common autoimmune disease and, despite decades of research, the death rate among sufferers remains about the same as it was when research began. The disease is caused when someone's immune system attacks her own joints, which inflames and thickens the synovial membranes surrounding the joints in a painful swelling that can then damage cartilage.

A study by Mariana Kaplan of the National Institute of Arthritis and Musculoskeletal and Skin Diseases and her colleagues examined how the immune system responds to joint injury. Neutrophils, a type of defensive white blood cells, migrate to the joint and extrude a mesh called a neutrophil extracellular trap, into the spaces between cells. This works very well to trap pathogenic microbes, but in RA, neutrophil extracellular traps activate local cells called fibroblast-like synoviocytes, triggering the painful inflammation and joint damage characteristic of the disease.

In the current study, published in the journal Science Immunology on April 14, the researchers found that once on patrol, the fibroblast-like synoviocytes absorb certain amino acid chains, or peptides, from the neutrophil extracellular trap that have a citrulline molecule attached—which happens to be the molecule that gives watermelon its characteristic taste. Once the fibroblast-like synoviocytes have swallowed the citrullinated peptides, the body’s immune system recognizes them as dangerous enemies. T cells and B cells attack, ramping up the severity and progression of the disease. As a further demonstration of this mechanism, the researchers also injected mice genetically engineered to be susceptible to inflammatory arthritis with citrullinated peptide-bearing fibroblast-like synoviocytes. The mice developed cartilage damage and loss.

The next step, said Kaplan, is to further explore the interactions between neutrophils and fibroblasts, “and test novel targets…that could have therapeutic effects in RA and other conditions.”