Researchers at Johns Hopkins Medicine have identified a biological mechanism that may help explain how inflammation is initiated and sustained in several diseases, with findings pointing to human resistin as a key regulator of the inflammatory response.

Published in PLOS One, the study found that human resistin activates the NLRP3 inflammasome, a major inflammatory pathway associated with conditions including cardiovascular disease, diabetes and autoimmune disorders. The researchers found that resistin helps prepare and activate immune cells known as macrophages, triggering a series of molecular events that leads to the release of inflammatory molecules, including IL-1β and IL-18.

The researchers also examined lung tissue from patients with pulmonary hypertension and observed increased activity of both resistin and the inflammasome pathway. According to the study team, the finding provides evidence that the mechanism observed in laboratory experiments may also be relevant to human disease.

The study further showed that blocking resistin with a targeted antibody reduced activation of the NLRP3 inflammasome pathway. This finding suggests that resistin could be investigated as a potential therapeutic target for regulating excessive inflammatory responses.

The researchers noted that further studies will be required to establish the therapeutic potential of targeting resistin and determine whether the mechanism can be applied across different inflammatory diseases.