Senescent Cells Promote Viral Infection-Associated Inflammation And Tissue Damage Through A Robust NF-Κb Pathway
Have you ever wondered why viral infections, like the flu or COVID-19, often hit older people harder, leading to more severe inflammation and organ damage? Recent research sheds light on this phenomenon by pinpointing a key culprit: senescent cells. These are “aged” cells that have stopped dividing but remain metabolically active and accumulate in our bodies as we get older. While seemingly harmless, they play a crucial role in ramping up the body’s inflammatory response to viruses.
This study found that these senescent cells promote severe inflammation and tissue damage during viral infections by significantly activating a molecular pathway called NF-κB. Think of NF-κB as a central command system for inflammation within our cells; when it’s overactive, it leads to an excessive release of inflammatory signals. The research delved deeper, discovering that this heightened NF-κB activity in senescent cells is due to an accumulation of harmful byproducts called reactive oxygen species and a reduced amount of a protein named PDLIM2. PDLIM2 is important because it normally helps control the NF-κB pathway, preventing it from going into overdrive.
Remarkably, when scientists restored the levels of PDLIM2, it significantly dampened the inflammation and protected against organ damage caused by viral infections in aged subjects. This breakthrough provides a novel understanding of why elderly individuals are more susceptible to severe viral infections and opens new avenues for developing treatments that could mitigate the devastating inflammatory “cytokine storms” often seen in these patients.
Source: link to paper