Researchers Identify Inflammatory Mechanism Related to Bone Damage in Rheumatoid Arthritis

A study published in Proceedings of the National Academy of Sciences details a novel path in the inflammatory mechanism associated with the bone damage caused by rheumatoid arthritis, reports News-Medical . The process involves the release by T-lymphocytes of extracellular vesicles packed with genetic material (microRNAs), which penetrate cells in bone tissue, boosting the formation of osteoclasts that break down bone matrix in joints. Earlier research illustrated that cigarette smoke worsens the inflammatory process in arthritis by triggering the aryl hydrocarbon receptor (AhR) on Th17 cells. The latest research indicated that the microRNA miR-132 in Th17 cells was more expressed due to AhR activation. "When we treated T-cells with antagonists of the microRNAs, they continued to differentiate normally into Th17 cells, releasing the cytokines characteristic of the inflammatory process in rheumatoid arthritis," said Paula Donate at the University of São Paulo's Center for Research on Inflammatory Diseases. When the researchers isolated extracellular vesicles emitted by Th17 and studied them in vitro, they found that the large amounts of miR-132 bundled in extracellular vesicles acted as inflammatory mediators, causing differentiation of osteoclasts by inhibiting the enzyme cyclooxygenase 2. "In the case of Th17 cells, the vesicles released in joints can transport microRNAs to bone tissue, augmenting the quantity of osteoclasts and bone erosion," Donate said. "In sum, this is a previously unknown mechanism that we succeeded in elucidating and that, in the future, could be a basis for novel therapies for joint injury."