ARE YOU AS OLD AS WHAT YOU EAT
Researchers from UCL
(University College London) have demonstrated how an interplay between
nutrition, metabolism and immunity is involved in the process of aging
The two new studies,
supported by the Biotechnology and Biological Sciences Research Council
(BBSRC), could help to enhance our immunity to disease through dietary
intervention and help make existing immune system therapies more effective.
As we age our immune
systems decline. Older people suffer from increased incidence and severity of
both infections and cancer. In addition, vaccination becomes less efficient
with age.
In previous BBSRC
funded work, Professor Arne Akbar's group at UCL showed that aging in immune
system cells known as 'T lymphocytes' was controlled by a molecule called 'p38
MAPK' that acts as a brake to prevent certain cellular functions.
They found that this
braking action could be reversed by using a p38 MAPK inhibitor, suggesting the
possibility of rejuvenating old T cells using drug treatment.
In a new study
published in Nature Immunology the group shows that p38 MAPK
is activated by low nutrient levels, coupled with signals associated with age,
or senescence, within the cell.
It has been suspected
for a long time that nutrition, metabolism and immunity are linked and this
paper provides a prototype mechanism of how nutrient and senescence signals
converge to regulate the function of T lymphocytes.
The study also
suggests that the function of old T lymphocytes could be reconstituted by
blocking one of several molecules involved in the process. The research was
conducted at UCL alongside colleagues from Complejo Hospitalario de Navarra,
Pamplona, Spain.
The second paper,
published in The Journal of Clinical Investigation, showed that blocking p38
MAPK boosted the fitness of cells that had shown signs of aging; improving the
function of mitochondria (the cellular batteries) and enhancing their ability
to divide.
Extra energy for the
cell to divide was generated by the recycling of intracellular molecules, a
process known as autophagy. This highlights the existence of a common signaling
pathway in old/senescent T lymphocytes that controls their immune function as
well as metabolism, further underscoring the intimate association between aging
and metabolism of T lymphocytes.
This study was
conducted by researchers from UCL, Cancer Research UK, University of Oxford and
University of Tor Vergata, Rome, Italy.
Professor Arne Akbar
said: "Our life expectancy at birth is now twice as long as it was 150
years ago and our lifespans are on the increase. Healthcare costs associated
with aging are immense and there will be an increasing number of older people
in our population who will have a lower quality of life due in part to immune
decline. It is therefore essential to understand reasons why immunity decreases
and whether it is possible to counteract some of these changes.
"An important
question is whether this knowledge can be used to enhance immunity during
aging. Many drug companies have already developed p38 inhibitors in attempts to
treat inflammatory diseases. One new possibility for their use is that these
compounds could be used to enhance immunity in older subjects. Another
possibility is that dietary instead of drug intervention could be used to
enhance immunity since metabolism and senescence are two sides of the same
coin."
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