“Feed a cold, starve a fever,” so the old saying goes, and according to a new study, it may hold some truth. Researchers found that mice with a bacterial infection died after being fed, while mice with a viral infection survived after eating.
Senior author Ruslan Medzhitov – David W. Wallace professor of immunobiology and a Howard Hughes Medical Institute investigator at Yale School of Medicine in New Haven, CT – and team report their findings in the journal Cell.
According to Medzhitov, most of our knowledge about bacterial and viral infections stems from studies that have investigated how the immune system responds to pathogens and how it works to eradicate them.
“But that’s not the only way we defend ourselves,” he notes. “There are also cases where we change and adapt so that microbes don’t cause harm.”
In the case of this latest study, the team found that food intake during infection may influence the immune system’s ability to fight pathogens, depending on whether the infection is bacterial or viral and what type of foods are consumed.
“We were surprised at how profound the effects of feeding were, both positive and negative,” says Medzhitov. “Our findings show that it has a strong protective effect with certain infections, but not with others.”
The researchers came to their findings by conducting a series of mouse experiments, in which they fed or starved mice that had been infected with bacteria or viruses.
Firstly, the team infected mice with Listeria monocytogenes – a bacterium known to cause food poisoning.
As expected, the mice stopped eating – a common occurrence with food poisoning – and eventually, they made a full recovery. However, when mice infected with L. monocytogenes were force-fed, they died.
On further investigation into the effects of each food component, the team found that it was glucose that proved fatal to the force-fed mice; proteins and fats appeared to have no effect.
What is more, on administering the chemical 2-DG – which inhibits glucose metabolism – to force-fed infected mice, glucose no longer proved fatal.
In another experiment, the team infected mice with the flu virus A/WSN/33.
Contrary to the results of the previous experiment, the team found that force-feeding the mice with glucose led to their survival, but the rodents died when they were given 2-DG or were starved of glucose.
By analyzing the brain scans of the mice that died from either bacterial or viral infection, the team found that each infection affected different brain regions.
The researchers say this suggests that the metabolic requirements of the mice may be determined by what parts of their immune system are switched on.
“Our study manipulated the ability of these mice to tolerate and survive infection without doing anything that had an effect on the pathogens themselves,” explains Medzhitov.
The researchers are now in the process of investigating how changes in sleep patterns affect the immune system’s ability to stave off infection.
They also plan to conduct follow-up studies, which will investigate what pathways play a role in food preferences, in an attempt to explain certain food craving people have when they are ill.
In the meantime, Medzhitov and colleagues believe their current findings may have important implications for research into sepsis – a potentially fatal blood infection.
“Sepsis is a critical problem in hospital ICUs that defies most modern medical approaches,” says Medzhitov.
“A number of studies have looked at nutrition in patients with sepsis, and the results have been mixed. But these studies didn’t segregate patients based on whether their sepsis was bacterial or viral. The implication is that patients should be stratified by the cause of their sepsis, and trials should be designed based on that.”