Posted on 11 August 2022
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.
Why is this research important: The blood stem cells within the bone marrow (hematopoietic stem cells) are capable of generating any of the different cell types found within the blood, including the white blood cells that make up our immune systems. These stem cells are also able to generate new stem cells in a process called self-renewal. Unfortunately, their self renewal ability declines with age, as does their ability to produce T cells and B cells, the ‘precision weapons’ of the immune system. Instead, these stem cells produce more of a group of white blood cells called granulocytes, which tend to cause collateral damage in their attempt to neutralise pathogens. Together, these lead to a weaker immune system in old age, and one that gradually damages the body’s own tissues over time. We think that these changes in the immune system are an important part of how we age, but why exactly do they happen to begin with?
What did the researchers do: In this study, researchers were intrigued by the fact that mice kept in conditions free of pathogens don’t seem to develop the kinds of blood diseases that are thought to be caused by ageing stem cells. They wanted to see if repeated infections had any permanent effects on the stem cells in the bone marrow. They took 8-16 week-old mice and gave them either an injection of bacteria, a substance to cause an inflammatory response, or a sham injection as a control. Mice received a varying number of injections separated by 4 week intervals. Researchers then painstakingly sampled and studied the blood stem cells in their bone marrow for up to 1 year following the treatments.
Key takeaway(s) from this research: The researchers found that each round of inflammation caused by either treatment had an additive effect on the mice’s stem cells, reducing their ability to produce a healthy population of blood cells. What’s more, these stem cells didn’t recover, even a year post-treatment.
It is currently thought that after dividing in response to an infection, blood stem cells enter a dormant state that maintains their ability to self-renew. However, the findings of the researchers here contradict that idea: they observed that after being forced to divide, stem cells failed to self renew. The consequences were similar to what is observed in the ageing humans, including a decline in blood cell numbers and in the number of stem cells in the bone marrow.
If inflammation has similar effects in humans, this strengthens the argument that anti inflammatory treatment throughout life might slow the ageing process. It may even be possible to restore the immune system to a more youthful state by reprogramming or completely replacing aged stem cells in the bone marrow.
Inflammatory exposure drives long-lived impairment of hematopoietic stem cell self-renewal activity and accelerated aging: https://doi.org/10.1016/j.stem.2022.06.012
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