Chronic or acute inflammation can contribute to a range of ailments—some potentially deadly—including stroke, respiratory and heart disease, cancer, arthritis, asthma, dementia, multiple sclerosis, and diabetes. In May, a study by Dr. Kate Lawlor and collaborator Professor Vince James (WEHI) published in Nature Communications shed light on the potential triggers of inflammation.

The research focused on the cytokine, interleukin-1ß (IL-1ß), which is critical to clearing infections but is also associated with sepsis and driving autoinflammatory and inflammatory diseases including rheumatoid arthritis, type 2 diabetes, and atherosclerosis.

Previous IL-1ß research had focused on understanding how it is triggered and how inhibiting this process or neutralizing IL-1ß could reduce inflammation. However, little was known about how the precursor IL-1ß protein is regulated.

The team discovered a key event that contributes to the depletion of inactive IL-1ß and limits access to the enzyme that activates IL-1ß. The potential trigger of inflammation discovery is a major step in understanding how IL-1ß levels could be manipulated to limit inflammatory responses and developing treatments for diseases associated with excessive inflammation.