Scientists at the Medical Research Council (MRC) Laboratory of Medical Science and Imperial College London have discovered that turning off a protein called IL-11 can significantly increase the healthy lifespan of mice by almost 25%.
In collaboration with colleagues at Duke-NUS Medical School in Singapore, the researchers tested the effects of IL-11 by creating mice that lacked the gene responsible for producing IL-11 (interleukin 11).
These mice lived over 20% longer on average.
The researchers also treated 75-week-old mice—equivalent to about 55 years in humans—with an injection of an anti-IL-11 antibody, a drug that stops the effects of IL-11 in the body.
The results, published in the journal Nature, were impressive.
Mice given the anti-IL-11 drug from 75 weeks of age until death had their median lifespan extended by 22.4% in males and 25% in females.
On average, these mice lived for 155 weeks, compared with 120 weeks in untreated mice.
The treatment largely reduced deaths from cancer in the animals and also decreased diseases caused by fibrosis, chronic inflammation, and poor metabolism, which are common in aging. Very few side effects were observed.
Professor Stuart Cook, co-corresponding author from the MRC Laboratory of Medical Science, Imperial College London, and Duke-NUS Medical School in Singapore, said, “These findings are very exciting.
The treated mice had fewer cancers and were free from the usual signs of aging and frailty. We also saw reduced muscle wasting and improvement in muscle strength. In other words, the old mice receiving anti-IL-11 were healthier.”
Previous life-extending drugs often had poor side effects or did not work equally well in both sexes. They could extend life but not necessarily improve health. This is not the case for IL-11. While these findings are only in mice, it raises the exciting possibility that the drugs could have a similar effect in elderly humans.
Anti-IL-11 treatments are currently in human clinical trials for other conditions, potentially offering new opportunities to study their effects on aging humans in the future.
The researchers have been investigating IL-11 for many years. In 2018, they were the first to show that IL-11 is a pro-fibrotic and pro-inflammatory protein, overturning years of incorrect beliefs that it was anti-fibrotic and anti-inflammatory.
Assistant Professor Anissa Widjaja, co-corresponding author from Duke-NUS Medical School, said, “This project started back in 2017 when a collaborator sent us some tissue samples for another project.
Out of curiosity, I ran some experiments to check for IL-11 levels. From the readings, we could clearly see that the levels of IL-11 increased with age, and that’s when we got really excited!”
They found that rising levels of IL-11 contribute to negative effects in the body, such as inflammation and preventing organs from healing and regenerating after injury. Although their work was done in mice, they hope these findings will be relevant to human health, as similar effects have been observed in studies of human cells and tissues.
Professor Cook added, “The IL-11 gene activity increases in all tissues in the mouse with age. When it gets turned on, it causes multimorbidity—diseases of aging and loss of function across the whole body.”
Multimorbidity and frailty are major global health care challenges. Currently, there is no treatment for multimorbidity other than addressing each condition individually.
The scientists caution that while the results in this study are promising, the safety and effectiveness of these treatments in humans need further study in clinical trials before anti-IL-11 drugs can be considered for this purpose.
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