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Longevity

Longevity Briefs: Antibodies Extend Mouse Lifespan By 25%. Will They Work In Humans?

Posted on 18 July 2024

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Longevity briefs provides a short summary of novel research in biology, medicine, or biotechnology that caught the attention of our researchers in Oxford, due to its potential to improve our health, wellbeing, and longevity.

The problem:

Inflammation appears to be a key component of the ageing process. Inflammation is supposed to occur in response to infection or injury as the body’s first line of defence against pathogens. Yet as we age, inflammation increasingly occurs when and where it should not, in the absence of any pathogens. This constant chronic inflammation is sometimes called inflammageing by scientists.

There are many molecules within our bodies that control inflammation, including a group called interleukins (ILs). IL-11 is one such molecule. It activates key signalling pathways thought to be involved in ageing and promotes cellular senescence (a hallmark of ageing in which cells are unable to divide). Research also shows that IL-11 levels increase with age in humans. For these reasons, researchers were interested in investigating whether IL-11 could be targeted to slow ageing in animals.

The discovery:

In this study, researchers found that inhibiting IL-11 signalling can significantly extend both lifespan and healthspan (the amount of time spent in good health) in mice. In their groundwork, they show that IL-11 levels do indeed increase in ageing mice, leading to cellular senescence, and that the signalling pathways involved are similar to those in human cells. They then deleted the IL11 gene, rendering mice unable to produce IL-11, and found that this was associated with a number of metabolic improvements (such as reduced liver fat), improved muscle function, increased telomere length and a reduced incidence of cancer in old mice when compared to equally aged unmodified mice. The median lifespan (the age by which 50% of mice are dead) increased by about 30 weeks in the modified mice, which is roughly a 25% increase.

Survival of mice lacking IL-11 (Il11-/-, yellow) and control mice (WT, black) over time.
Inhibition of IL-11 signalling extends mammalian healthspan and lifespan
https://doi.org/10.1038/s41586-024-07701-9

Genetically deleting IL11 wouldn’t be a viable way to target ageing in humans, and the results of doing so are confounded by the fact that ILs play a role in controlling embryonic development, which could have been affected by the deletion. The researchers wanted to see if they could improve the health of mice that were already old by targeting IL-11. To do this, they gave them an antibody targeting IL-11 when they were 75 weeks old (this can be roughly equated to 55 ‘human years’). They found that the benefits were very similar to those of deleting the IL11 gene, including the 25% increase in median lifespan.

Survival of mice given anti-IL-11 (blue) and control mice (IgG, black) over time. The red dotted line represents the administration of anti-IL-11 or control treatment.
Inhibition of IL-11 signalling extends mammalian healthspan and lifespan
https://doi.org/10.1038/s41586-024-07701-9

The implications:

Could we use a similar strategy to improve health and lifespan in humans? The good news is that anti-IL-11 for humans already exists, is currently in clinical trials for the treatment of fibrotic lung disease, and so far appears to be safe. But can it combat age-related deterioration in older adults? The benefits of treatments that modulate ageing tend to diminish in organisms that are more complex, and that’s likely to apply in this case – a 25% increase in median lifespan would obviously be an exceptional achievement in humans. However, even if anti-IL-11 doesn’t increase lifespan at all, it could still be very valuable if it can extend healthspan, for example by improving fat distribution and muscle function, and by reducing frailty.

Unfortunately, this study used C57BL/6 (aka black 6) mice, a strain of inbred mice that develop a lot of health problems and therefore don’t make for great models of human ageing. Hopefully these results can be replicated in genetically healthy mice.


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    References

    Inhibition of IL-11 signalling extends mammalian healthspan and lifespan https://doi.org/10.1038/s41586-024-07701-9

    Image by pikisuperstar on Freepik

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