Tuesday, September 29, 2020

PEG-PLGA from PolySciTech used in development of arthritis treatment

 

Arthritis is a disease in which the cartilidge in joints begins to break down leading to severe damage and pain. This disease is driven by a pathological immune imbalance in which the immune system starts attacking at the sight of the cartilidge leading to severe inflammation. Recently, researchers at University of Pittsburgh used PEG-PLGA (AK037) from PolySciTech (www.polyscitech.com) to create a delivery system to decrease the hyperactive immune response in joints and reduce the progression of arthritis. This research holds promise to prevent this potentially debilitating disease. Read more: Bassin, Ethan J., Abigail R. Buckley, Jon D. Piganelli, and Steven R. Little. "TRI microparticles prevent inflammatory arthritis in a collagen-induced arthritis model." PloS one 15, no. 9 (2020): e0239396. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0239396

“Abstract: Despite recent progress in the treatment of rheumatoid arthritis (RA), many patients still fail to achieve remission or low disease activity. An imbalance between auto-reactive effector T cells (Teff) and regulatory T cells (Treg) may contribute to joint inflammation and damage in RA. Therefore, restoring this balance is a promising approach for the treatment of inflammatory arthritis. Accordingly, our group has previously shown that the combination of TGF-β-releasing microparticles (MP), rapamycin-releasing MP, and IL-2-releasing MP (TRI MP) can effectively increase the ratio of Tregs to Teff in vivo and provide disease protection in several preclinical models. In this study TRI MP was evaluated in the collagen-induced arthritis (CIA) model. Although this formulation has been tested previously in models of destructive inflammation and transplantation, this is the first model of autoimmunity for which this therapy has been applied. In this context, TRI MP effectively reduced arthritis incidence, the severity of arthritis scores, and bone erosion. The proposed mechanism of action includes not only reducing CD4+ T cell proliferation, but also expanding a regulatory population in the periphery soon after TRI MP administration. These changes were reflected in the CD4+ T cell population that infiltrated the paws at the onset of arthritis and were associated with a reduction of immune infiltrate and inflammatory myeloid cells in the paws. TRI MP administration also reduced the titer of collagen antibodies, however the contribution of this reduced titer to disease protection remains uncertain since there was no correlation between collagen antibody titer and arthritis score.”

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