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 Associate Professor 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 neutralising IL-1ß could reduce inflammation. However, little was known about how the precursor IL-1ß protein is regulated.
Inflammatory disease treatments
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.
Collaborators | Monash University; University of Melbourne; WEHI
Funders | National Health and Medical Research Council (NHMRC)
Contact us
Hudson Institute communications
t: + 61 3 8572 2761
e: communications@hudson.org.au
