A quick overview of what you’ll learn from this blog post:
- What is altered intercellular communication?
- How it happens
- The consequences of altered intercellular communication
The Hallmarks of Aging describes altered intercellular communication as an alteration of the signals that pass between cells. These changes to how cells communicate can lead to various age-related diseases and disabilities.
Chronic inflammation disrupts cell-to-cell communication
Cells do not exist in isolation; they actually talk to each other. They signal to each other using chemical messages which lets them talk to both near and distant cells. In this way our cells can coordinate their efforts and allow us to function as living beings.
Unfortunately, as we grow older this cell-to-cell communication system begins to go wrong. The chemical messages across the entire body become increasingly more pro-inflammatory in nature and the level of chronic inflammation rises. This smoldering, persistent inflammation that typically accompanies advancing age is known as inflammaging.
It causes cells to behave differently and often in a harmful manner and for maintenance systems to break down. This in turn hampers the immune system from working properly, interferes with stem cell function and tissue regeneration, supports muscle and bone loss.
How does altered intercellular communication happen?
Inflammaging has various sources including those listed below.
- Changes to our gut microbiome
- Cell debris
- Senescent cell accumulation
- Immunosenescence
Changes to our gut microbiome can contribute to altered intercellular communication. Our gut is home to an ecosystem of bacteria, archaea, viruses, and fungi known collectively as the microbiome. These microorganisms can be symbiotic or pathogenic in nature and as we age the microbiome shifts increasing in favor of the latter. These changes promote inflammation and immune system dysfunction.
Cell debris is the organic waste that remains after a cell dies and is an inevitable consequence of the life-cycle of cells. Under normal circumstances our immune system clears away this waste, but as we age and the immune system begins to fail, this removal process slows down. Ultimately this leads to an increasing amount of organic waste lying around which contributes to inflammation.
Senescent cell accumulation is another hallmark of aging which has an impact on intercellular communication and highlights how interconnected the aging processes are. Senescent cells secrete a pro-inflammatory cocktail of chemical messages known as the senescence-associated secretory phenotype (SASP). As we age more and more of these problem cells accumulate and the level of SASP rises. The SASP disrupts cell-to-cell communication and promotes chronic inflammation.
Immunosenescence describes the age-related decline of the immune system. It is typically associated with inappropriate immune responses which then contribute to the chronic inflammation that accompanies aging. Immunosenescence reduces our ability to respond to pathogens, makes us more vulnerable to infections, increases the risk of autoimmune reactions, and puts us at higher risk for cancer. It also reduces our response to vaccinations and impairs wound healing.
What can we do about altered intercellular communication?
In general approaches that reduce global inflammation should help with this hallmark. The most hands on approach available to us all now is caloric restriction or diets that mimic it. While the data is currently inconclusive that caloric restriction increases lifespan in humans, it does seem to have a number of benefits including reducing inflammation.
- Next gen plasma exchange
- Neutral Blood exchange
- Approaches that remove or block senescent cell SASP
- Boosting the immune system so it clears cell debris
- Reducing chronic inflammation
- Caloric restriction or diets that mimic it
It might seem that this hallmark is a problem that is too complex to solve, but the good news is that it might not be. Because this hallmark is linked directly to some of the others, such as cellular senescence, addressing that could also help. Researchers are busy developing solutions to this and other hallmarks and so solving one could have a knock on effect.