Senescent Cells Make Lungs More Susceptible to Infection

Senescent cells build up in our tissues with age. They have left the cell cycle, damaged and dysfunctional, fail to self-destruct through one of the many systems for cell suicide, and linger on to cause all sorts of problems for their neighbors. Tissue riddled with senescent cells is less effective, less resilient, and more prone to developing further damage.

One of the roles of the immune system is to clear out these problem cells, but the immune system itself progressively fails in all its tasks with age, a victim of its own issues. So the senescent cell population grows, promoted by increasing levels of damage caused by the other processes of aging, and the immune system fails to rein it in.

Here, researchers demonstrate one specific result of an increased population of senescent cells: an additional susceptibility to lung infection over and above the issues caused by an age-damaged immune system.

The researchers found that when it comes to aging and pneumonia, one bad apple can ruin the barrel. Lung cells that were supposed to die due to DNA damage - but didn't - were 5 to 15 times more susceptible to invasion by pneumonia-causing bacteria. These bad apples also increased the susceptibility of normal cells around them.

Both age and [pneumonia] are associated with senescent cells, which are unable to die due to dysregulated function. These cells have increased levels of proteins that disease-causing bacteria stick to and co-opt to invade the bloodstream. The cells also spew out molecules that increase inflammation, and make normal cells nearby do the same.

How will we deal with senescent cells with near future biotechnology? The likely answer is through the use of technologies pioneered in cancer research: precision cell-killing strategies that can locate and destroy very specific types of cell without harming any other cell types. These may use nanoparticles or they may involve training the immune system to attack senescent cells with vigor, but both paths have been demonstrated effective in the laboratory.

Sadly, as for so much of what might be done, next to no-one is actually working on adapting these developing technologies for use against senescent cells. That's one more thing to add to the long term to-do list for Open Cures and a strategy of promoting overseas development of new biotechnologies.

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