One question this gives rise to is whether chronic inflammation is a cause of aging or if it is a consequence of the aging process itself. Researchers at the Max Planck Institute for Biology of Aging in Germany have found evidence that increased inflammation causes the aging process to speed up, and that there is a delicate balance between maintaining immune system function and longevity.
The researchers describe their work published on ELifeSciences in which they discovered a change in an evolutionarily conserved gene named PUF60 during work with C.elegans that made the worms live 20% longer but at the same time dampened their immune response to succumb more quickly to infection. This suggests that an overactive immune system can shorten lifespan, but a less active immune system can increase lifespan.
PUF60 works as a splicing factor to help regulate the balance between the immune system and longevity, and it is also involved in the removal of segments in the ribonucleic acid which is essential to generate functional proteins. Genetically changed PUF60 were found to disturb this process and alter the regulation of other genes that are involved in immune functions. Thus lysosome to mitochondria communication may regulate longevity.
“We’re excited by this finding because it implicates a very fundamental process in the cell to immunity,” says Adam Antebi. “These observations of course raise further questions. Notably pinpointing how PUF60 activity affects immunity and longevity, and how these two processes are balanced will be central to understanding the relationship between inflammation and aging.”
