endotoxin. “The mice without the gene died due to an uncontrolled septic-shock like response—their blood vessels burst, their spleens were destroyed,” says Dr. Schneider. Mortality was five-fold higher in mice without the auf1 gene.
Further research showed where auf1 functions at the molecular level, he says. In normal mice, the scientists found that auf1 steps into action once the immune response is activated and after cytokine production gets underway. The action is pronounced: messenger RNAs (mRNAs) which are blueprints for very specific cytokines—namely interleukin-1 beta, tumor necrosis factor alpha and COX-2—are degraded. That process of degrading the mRNAs shuts off production of these cytokines.
In the study, mice lacking the auf1 gene do not seem to have that off switch; their cytokine levels were greatly elevated. A cytokine storm had caused sepsis in these animals.
In summary, auf1 is a protector that can stop an infection from progressing to septic shock, explains Dr. Schneider. It does so by helping with cytokine production and then tempering the production of these proteins. Auf1 acts like a cytokine on/off switch.
The future possibilities
Dr. Schneider believes auf1 makes an excellent target for the development of therapeutics. For example, a drug could turn on auf1 or stabilize its activity as a way to specifically tone down production of those cytokines that are the major players in sepsis, he says. His study results might also help explain why many previous sepsis drug trials have failed. The cytokine storm needs to be turned off at its source, he says, and auf1 offers the on/off switch to do just that.
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