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The end of inflammation? New approach could treat dozens of diseases.
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The end of inflammation? New approach could treat dozens of diseases.
The end of inflammation? New approach could treat dozens of diseases.
Cancer, aging, and severe COVID-19 have all been linked to damage from inflammation. Now scientists are flipping their focus to find new drugs that may revolutionize treatments.
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“Simply stopping inflammation is not enough to return tissue to its normal state,” says Ruslan Medzhitov, a professor of immunobiology at Yale School of Medicine. This approach ignores the other side of the inflammation coin: resolution. Resolving inflammation is an active, highly choreographed process for rebuilding tissue and removing the dead bacteria and cells. When that process is disrupted, inflammatory diseases arise.”
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“In mice with diabetic kidney disease, scarring from kidney inflammation gradually destroys the organ. Her team is testing the therapeutic potential of a lipoxin mimetic in these and other animal models. They’ve also looked at the mimetic’s effect in human tissue in lab cell cultures taken from patients with atherosclerosis, an inflammatory disease of the blood vessel wall. In both cases, inflammatory factors plummeted when the mimetic was introduced; for the mice, the kidneys recovered their function in a stunning reversal of established disease.”
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“Macrophages start to produce factors that tell the local tissue, Don’t recruit any more inflammatory cells here, or, Let’s proliferate and start repairs there,” says Kodi Ravichandran, an immunologist at Washington University in St. Louis whose research focuses on how dead cells are cleared from the body.
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““If you knock out receptors in the macrophages of mice that recognize dying cells, for example, they become incapable of eating up these cells, resulting in a lupus-like disease,” with symptoms such as arthritis and skin rash, says Krönke.
A similar mechanism is at work in older people, says Gilroy. As we age, the body loses a protein that recognizes dying cells; this blocks macrophages’ ability to find and eat debris. Locked in a pro-inflammatory state, these macrophages continue to produce molecules that amplify the inflammatory response early on.”
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“Chemotherapy and radiation are like sledgehammers,” Panigrahy says. “They may kill the tumor, but the debris they create stimulates inflammation, which feeds circulating tumor cells that survive the treatment.”
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But Gilroy cautions that the answer may be more nuanced than anti-inflammatory versus pro-resolution, and that drugs targeting both approaches may be needed.
“It’s like driving a car at full speed,” he says. “In order to stop, you take your foot off the accelerator, which would be like dampening inflammation’s onset. And then you apply the brakes, or in other words, promote its resolution.”
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