Researchers here provide evidence suggesting that one of the mechanisms by which senescent cells encourage nearby cells to also become senescent is via recruitment of neutrophil cells, a somewhat more complicated process than the direct signaling investigated to date. In its role as a suppressor of cancer, it makes sense for the state of cellular senescence to be transmissible to nearby cells, as that raises the chances of successfully preventing cancer from arising in a localized environment of cell damage. In aging, it makes things worse, however. Excessive numbers of lingering senescent cells cause harm to their surroundings and make that harm worse over time via the creation of yet more senescent cells.
The immune system is a collection of cells and proteins that works to keep the body healthy. But it's a balancing act. Tip in one direction and an infection might cause organ damage or lead to sepsis. Overbalance in the other and the cure might lead to an autoimmune disease. Neutrophils are a key part of immune system action. They help healing by clearing out cellular debris after an infection. They're also armed and can kill microbes. During infection, neutrophils release a short blast of unstable molecules called reactive oxygen species.
Another way the immune system keeps the body healthy is by telling damaged cells to perish. But not all cells die. Cells told to close down by the body sometime ignore that signal. Instead, they live in a sort of zombie state, undead but spewing toxic chemicals. These cells are senescent cells. They damage their neighbors through release of a toxic protein stew.
Researchers examined neutrophils' effect on human and mouse cell senescence. They co-cultured neutrophils with human cells and depleted neutrophils in mice to determine their role in encouraging senescence. "We asked if neutrophils could be drivers of cellular senescence in tissues and contribute to aging. We found that neutrophils can cause senescence in neighboring non-immune cells by damaging their telomeres via reactive oxygen species. We also found that if we deplete neutrophils in mice, we can prevent telomere damage and senescence. Our study suggests an evolutionary trade-off between having a good working immune system and age-related pathology. While neutrophils have evolved to play important roles in fighting infection, they may contribute to collateral damage and induction of cellular senescence which will be detrimental later in life."