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New engineered drug may offer prolonged arthritis relief

an weaken the immune system and make patients more susceptible to infection.

Such vulnerability to infection is a particular problem for patients treated for chronic diseases such as osteoarthritis, and this vulnerability suggests the need for a local treatment, Shamji added.

Based on the initial investigation, the team paired the ELP with the IL1RA drug in a second study, to test whether the fusion protein would retain the ability to suppress IL-1 activity and fight inflammation.

The researchers treated human white blood cells with either the original or the modified drug. White blood cells are responsible for mounting the body's immune response and normally react to IL-1 by growing in numbers and releasing molecules that further activate the immune system. Active IL1RA therefore serves to dampen the immune cells' rate of proliferation, Shamji said.

White blood cells treated with the modified drug increased in number at a slower than normal pace, evidence of the drug's activity, Shamji reported at the Biomedical Engineering Society meeting. But its potency dropped by a factor of about 20 compared to the pure drug.

Further studies, however, suggested the fusion protein might do better in an arthritic joint, Shamji said. The researchers were surprised to find that the same inflammatory enzymes that destroy joint collagen also chew ELP from the original drug protein, thereby restoring its activity.

"With the ELP tag gone, you get back your originally active drug," Shamji said.

"That finding was pretty unexpected," Setton added. "We hadn't intentionally designed it to have that feature at all."

The researchers now plan to work with collaborators to test the modified drug's ability to interfere with the progression of disease in the joints of animals.


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Source:Duke University


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