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.
More information:
Swarna L. Vijayaraj et al, The ubiquitylation of IL-1β limits its cleavage by caspase-1 and targets it for proteasomal degradation, Nature Communications (2021). DOI: 10.1038/s41467-021-22979-3
Citation:
Finding the triggers of inflammation (2022, July 12)
retrieved 26 April 2024
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