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Finding a new way to fight late-stage sepsis by boosting cells' antibacterial properties:
Researchers have developed a way to prop up a struggling immune system to enable its fight against sepsis, a deadly condition resulting from the body's extreme reaction to infection.
The scientists used nanotechnology to transform donated healthy immune cells into a drug with enhanced power to kill bacteria.
In experiments treating mice with sepsis, the engineered immune cells eliminated bacteria in blood and major organs, dramatically improving survival rates.
This work focuses on a treatment for late-stage sepsis, when the immune system is compromised and unable to clear invading bacteria. The scientists are collaborating with clinicians specializing in sepsis treatment to accelerate the drug-development process.
"Sepsis remains the leading cause of death in hospitals. There hasn't been an effective treatment for late-stage sepsis for a long time. We're thinking this cell therapy can help patients who get to the late stage of sepsis," said Yizhou Dong, senior author and associate professor of pharmaceutics and pharmacology at The Ohio State University. "For translation in the clinic, we believe this could be used in combination with current intensive-care treatment for sepsis patients."
The study is published today in Nature Nanotechnology.
Sepsis itself is not an infection—it's a life-threatening systemic response to infection that can lead to tissue damage, organ failure and death, according to The Centers for Disease Control and Prevention. The CDC estimates that 1.7 million adults in the United States develop sepsis each year, and one in three patients who die in a hospital have sepsis.
This work combined two primary types of technology: using vitamins as the main component in making lipid nanoparticles, and using those nanoparticles to capitalize on natural cell processes in the creation of a new antibacterial drug. Cells called macrophages are one of the first responders in the immune system, with the job of "eating" invading pathogens. However, in patients with sepsis, the number of macrophages and other immune cells are lower than normal and they don't function as they should.
Journal Reference:
Xucheng Hou, Xinfu Zhang, Weiyu Zhao, Chunxi Zeng, Binbin Deng, David W. McComb, Shi Du, Chengxiang Zhang, Wenqing Li, Yizhou Dong, Vitamin lipid nanoparticles enable adoptive macrophage transfer for the treatment of multidrug-resistant bacterial sepsis, Nature Nanotechnology (2020). DOI: 10.1038/s41565-019-0600-1 , https://nature.com/articles/s41565-019-0600-1
(Score: 1, Interesting) by Anonymous Coward on Wednesday January 08 2020, @05:40PM
It's a reducing agent. Anaerobes only grow if the redox potential of their environment is sufficiently low (roughly less than +60-100 mV), so in that case we would expect it to stimulate growth. The reverse is true for aerobic bacteria though, they only grow if the potential is *high* enough. In that case ascorbate acts as a bacteriostatic agent.
It also reduces ferric (Fe3+) to ferrous (Fe2+) iron. Ferrous iron reacts with oxygen to form superoxide radical, and with hydrogen peroxide to form hydroxyl radical (ie, the fenton reaction). Same with copper. Thus, ascorbate can act as a source of electrons to replenish ferric iron levels and generate free radicals which are bacteriocidal. Now, ascorbate can also quench these free radicals so how it all works out depends on the concentrations involved.
This has been known since like the 1930s, but you can find many more recent papers on this if you look.
Correct, it is not magic. It is the best reducing agent in the universe at physiological pH because its first stage oxidation product is the exceptionally long lived resonance stabilized ascorbate radical. This is *also* a great reducing agent, upon which you get dehydroascorbate. This is also a great molecule because it can be easily recycled back to ascorbate by glutathione, but if not is quickly hydrolyzed to a non-oxidant compound (2,3-diketo-L-gluconic acid).
Thus *anywhere there are excess free radicals vitamin c acts as a great nontoxic source of electrons*. The end result is non-toxic compounds and lipids and proteins that have been saved from oxidative damage. This is why when *sufficient* amounts of vitamin c reach an inflamed tissue the symptoms of inflammation and threat of structural damage is reduced. So it helps *anywhere free radicals and inflammation is a problem*, which is basically every single illness.
I'll respond to this and the rest in a follow up.