A new study finds that 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. The failure of these bad cells to die also increased the susceptibility of normal cells around them to the same bacteria, according to findings published in the journal Aging Cell.
Close to 1 billion adults worldwide are at risk for pneumonia, including the more than 800 million adults who are older than 65 and an estimated 210 million with chronic obstructive pulmonary disease (COPD). Community-acquired pneumonia is the leading cause of infectious death among the elderly.
Both age and COPD 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 release molecules that increase inflammation, and make normal cells nearby do the same. Controlling the release of the inflammatory molecules could short-circuit the pneumonia risk in the elderly, according to the researchers.
“We can’t stop aging, but our findings suggest that preventing inflammation might be the next best thing,” said Carlos Orihuela, PhD, assistant professor of microbiology and immunology at the University of Texas Health Science Center San Antonio. “This opens up possibilities for anti-inflammatory drugs as treatments for pneumonia.”
For the study, the researchers compared aged and young mice, all healthy. The older mice were found to have increased lung inflammation with higher levels of senescence markers. These findings were consistent with previous studies in the literature.
The lung cells in the aged mice also proved to be more susceptible to infection by the bacteria Streptococcous pneumonia. This was determined by increased levels of proteins to which the bacteria adhere and by testing bacterial adhesion to the lung cells.
Four different experiments—on senescent cells, on normal lung cells exposed to senescent cells, on aged mice, and on young mice exposed to gene-damaging stress—revealed increased susceptibility to pneumonia infection.
Source: University of Texas Health Science Center at San Antonio