Inflammation is part of the body’s natural healing process. But when it becomes chronic, inflammation can lead to cancer, Alzheimer’s disease and other conditions. Inflammasomes — protein-based molecular machines — trigger inflammation in response to different signals generated by cell stress, tissue injury or infectious organisms.
In a study published online July 25 in the journal Nature, University of California San Diego School of Medicine researchers identified a signaling pathway that activates the NLRP3 inflammasome implicated in several severe chronic inflammatory disorders.
“It has been obvious for some time that, when available, drugs that turn off the NLRP3 inflammasome, but not other inflammasomes, will be very useful for treating a variety of inflammatory disorders, from osteoarthritis to Alzheimer’s disease and cancer,” said Zhenyu Zhong, PhD, first author and UC San Diego School of Medicine postdoctoral researcher. “Until now, it was not clearly understood how environmental stress and tissue injury activate the NLRP3 inflammasome and, without such knowledge, it was impossible to rationally design specific inhibitors of the NLRP3 inflammasome.”
Interleukin 1β (IL-1β) is an inflammatory cytokine or hormone responsible for beneficial and adverse effects of inflammation. Normally, IL-1β is produced in very low amounts, but in response to injury,
Article originally posted at