NLRP3 tagged posts

Whether cells in the human body survive or die under stress depends, among other things, on their mitochondria. Scientists at the Faculty of Medicine at the University of Freiburg have now shown that a sudden stop in energy production in mitochondria prevents normal cell death or so-called apoptosis and instead triggers an inflammatory response. The results of this research were published in the journal Immunity.

“We found that mitochondria provide a kind of decision-making aid: they regulate whether a cell undergoes clean, silent apoptosis or releases pro-inflammatory messenger substances,” explains Prof. Dr...

Researchers describe the biochemical pathway that results in the generation of oxidized mitochondrial DNA, how it is expelled by mitochondria and how it triggers the complex and destructive inflammatory response that follows.

Mitochondria are self-contained organelles (they possess their own mini-chromosome and DNA) residing within cells and are charged with the job of generating the chemical energy needed to fuel functions essential to life and well-being.

When stressed, damaged or dysfunctional, mitochondria expel their DNA (mtDNA), oxidized and cleaved, into the cyto...

Scientists detail new work on NLRP3, an intracellular complex that has been found to participate in melanoma-mediated inflammation, leading to tumor growth and progression. By inhibiting NLRP3, the researchers found, they can reduce inflammation and the resultant tumor expansion.

Cancer doctors may soon have a new tool for treating melanoma and other types of cancer, thanks to work being done by researchers at the University of Colorado Cancer Center.

Specifically, NLRP3 promotes inflammation by inducing the maturation and release of interleukin-1-beta, a cytokine that causes inflammation as part of the normal immune response to infection. In cancer, however, inflammation can cause tumors to grow and spread.

“NLRP3 is a member of a larger family that is involved in sensing da...

Compared with a control (left), treatment with a miR-223 mimetic (right) reduces inflammation in mouse intestine. Credit: Neudecker et al., 2017

An international team has discovered that a microRNA produced by certain white blood cells can prevent excessive inflammation in the intestine. The study, “Myeloid-derived miR-223 regulates intestinal inflammation via repression of the NLRP3 inflammasome,” shows that synthetic versions of this microRNA can reduce intestinal inflammation in mice and suggests a new therapeutic approach to treating patients with Crohn’s or ulcerative colitis.

Inflammatory bowel disease (IBD), including Crohn’s disease and ulcerative colitis, affects almost 2 million people in the US...