New research suggests that limiting the body’s inflammatory response during a bacterial infection may help fight off infection in older people. Although it may seem counter-intuitive, researchers believe this finding is crucial in tailoring anti-bacterial strategies according to the age of the patient.
“As we age, levels of inflammatory cytokines in the blood and tissues increase. Although this appears to be an inevitable part of aging, it ultimately contributes to declining health,” write the authors of the study “TNF Drives Monocyte Dysfunction with Age and Results in Impaired Anti-pneumococcal Immunity,” which was published in PLOS Pathogens.
Dr. Dawn Bowdish, assistant professor at McMaster University in Hamilton, Canada, and senior author of the study, along with her colleagues compared the immunity of younger and older mice. They saw that in the bone marrow and blood of older mice, there were higher numbers of monocytes, which are cells of the immune system that play a crucial role in inflammation. They also saw higher levels of the pro-inflammatory cytokines, TNF and IL-6. This was also the case in the blood of older humans.
When they infected the mice with pneumonia-causing bacteria, Streptococcus pneumoniae, they saw that the monocytes were not able to clear the bacteria as fast as in the younger mice. The researchers then went on to use drugs (or drug-infected mice) to reduce the number of monocytes and remove TNF. They saw that the immune system of the older mice got better at fighting off the bacteria in a similar way to the younger mice.
“Lowering levels of TNF may be an effective strategy in improving host defence against S. pneumoniae in older adults,” the authors concluded.
Monocytes are cells of the immune response that play a crucial role in inflammation. They are produced and mature in the bone marrow. Upon infection or injury, they enter the blood stream and are transported to the site of infection, where they differentiate into macrophages. The role of the macrophages is to digest and clear away bacteria, infected cells, and debris.
With age, the amount of the cell-signaling molecule TNF increases, causing the monocytes to leave the bone marrow before they have matured. These immature monocytes are not very good at fighting off bacteria. When the body is infected with bacteria, they produce even more inflammatory cytokines, causing even more monocytes to leave the bone marrow without maturing. The result is chronic low-level inflammation seen in the elderly. This so-called “inflamm-aging” has been associated with susceptibility to infection.
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