Changes in the immune system can promote healthy aging

Date:
July 10, 2020
Source:
Max-Planck-Gesellschaft
Summary:
As we age, the immune system gradually becomes impaired. One
aspect of this impairment is chronic inflammation in the elderly,
which means that the immune system is constantly active and
sends out inflammatory substances. Such chronic inflammation
is associated with multiple age- related diseases including
arthritis and Alzheimer's disease, and impaired immune responses
to infection. One of the questions in ageing research is whether
chronic inflammation is a cause of aging, or a consequence of the
aging process itself? Scientists have found evidence suggesting
that increased inflammation causes the aging process to speed up,
and that there is a fine balance between maintaining immune system
function and longevity.



FULL STORY ==========================================================================
As we age, the immune system gradually becomes impaired. One aspect
of this impairment is chronic inflammation in the elderly, which means
that the immune system is constantly active and sends out inflammatory substances. Such chronic inflammation is associated with multiple
age-related diseases including arthritis and Alzheimer's disease, and
impaired immune responses to infection.

One of the questions in ageing research is whether chronic inflammation
is a cause of ageing, or a consequence of the ageing process
itself? Scientists in the laboratory of Director Adam Antebi at the Max
Planck Institute for Biology of Ageing in Cologne, Germany have found
evidence suggesting that increased inflammation causes the ageing process
to speed up, and that there is a fine balance between maintaining immune
system function and longevity.


==========================================================================
From their work in the tiny roundworm, Caenorhabditis elegans, the
scientists discovered a change in an evolutionarily conserved gene called PUF60, which made the worms long lived but at the same time dampened
the immune response.

Worms with this change lived about 20% longer than normal worms, but when
they were infected with certain bacteria, they succumbed more quickly
to the infection. This means that an overactive immune system also has
a price: it shortens life span. Conversely, a less active immune system
pays off as longer life span -- as long as the animal does not die from
an infection.

How does PUF60 regulate this fine balance between a maintained immune
system and longevity? PUF60 works as a so-called "splicing factor," and is involved in the removal (or "splicing out") of segments in the ribonucleic acid, RNA. This process is essential to generate functional proteins.

The scientists found that the genetically changed PUF60 perturbs this
process and alters the regulation of other genes that are involved in
immune functions.

"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 ageing."

========================================================================== Story Source: Materials provided by Max-Planck-Gesellschaft. Note:
Content may be edited for style and length.


========================================================================== Journal Reference:
1. Chun Kew, Wenming Huang, Julia Fischer, Raja Ganesan, Nirmal
Robinson,
Adam Antebi. Evolutionarily conserved regulation of immunity by the
splicing factor RNP-6/PUF60. eLife, 2020; 9 DOI: 10.7554/eLife.57591 ==========================================================================

Link to news story: https://www.sciencedaily.com/releases/2020/07/200710121810.htm

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