As if colds and the flu aren't bad enough, a breakdown in communications between our brains and our immune systems may serve to prolong our agony as we get older, University of Illinois research indicates.
UI Professor Rod Johnson thinks aged microglial cells, key immune cells in the brain, overreact to signals from our body's immune system in response to pathogens.
The cells promote inflammation by secreting chemicals called cytokines, which makes us feel rotten and, accordingly, encourages us to get the rest we need to recover.
"These biochemical changes are normally very good," said Johnson, a professor of integrative immunology and behavior in the UI Animal Sciences Department.
But microglial cells already grow more likely to produce cytokines as they age – Johnson likened them to a primed pump – and the signals from the immune system about an illness may result in an excess of the chemicals, one possible reason older folks feel worse longer when they're sick.
In addition, the body maintains a balance between inflammatory and anti-inflammatory chemicals, and Johnson's research shows that production of at least one of the anti-inflammatories is curtailed with aging.
The bodies of older people also may be more prone to activating genes involved in inflammatory immune response, Johnson said.
Any of those factors, or more likely all of them in combination, may be why illnesses seem to linger longer as we age.
While Johnson doesn't study chronic diseases, he said research elsewhere, notably the United Kingdom, indicates that the processes leading to lingering cold and flu symptoms also might play into neurodegenerative disorders, such as Alzheimer's and Parkinson's diseases, and the general decline in cognitive function with aging.
Johnson's research focuses on why animals and people behave the way they do when they develop an infection.
The body's reaction is controlled by the brain, but the brain itself has no way to recognize the entrance of a pathogen. For that, it relies on the immune system and the warning signals it passes along.
In the case of livestock, problems with that process can lead to reduced growth, said Johnson, who's looked at the effect of inflammatory cytokines on animal growth.
Animals grown for food generally aren't around long enough for the effects of aging to be a problem. But it can be an issue with companion animals or pets, Johnson noted.
Johnson and colleagues reached their conclusions by exposing young adult and aged mice to a molecule present on E. coli and other bacteria, which strongly activated their immune response.
Like sick people, the sick mice exhibit such symptoms as decreased appetite, weight loss and a lack of interest in socializing with cage mates. The young mice recovered by the next day but the older mice still exhibited symptoms three to four days later.
The researchers also looked at the brains of the mice at the cellular level using a microarray, or "gene chip," to examine more than 39,000 genes. Johnson said the mice are a good model for the dealings of the human brain and immune system.
The results appeared this fall in the journal of the Federation of American Societies for Experimental Biology. UI Professor Keith Kelley, researchers Jing Chen and Jonathan Godbout and graduate students Jayne Abraham, Brian Berg and Amy Richwine, also contributed to the study, which was funded by the National Institutes of Health.
Johnson said the UI researchers are focusing now on the hippocampus, which plays a role in memory and spatial navigation and is sensitive to aging, and looking at such things as how an excess of cytokines may change the brain's cellular structure and make it less likely to form communications links.