You no doubt know that the Salmonella strain of bacteria can cause you to become seriously ill. But new research shows that the stomach-distressing bug has a vested interest in keeping you healthy, and uses a tricky mechanism to do so. In a way, it proves that the old saw about feeding a cold could be pretty good advice.
Researchers at the Salk Institute in California were interested in finding out why, when we get sick, our behavior changes. We can change our grooming habits, find it hard to sleep and, most significantly, we can lose our appetites, a strategy that helps the body conserve energy to fight off infection.
But in a study in which mice were infected with a strain of salmonella called Salmonella Typhimurium that causes a typhoid-like disease, they found that mice that were fed more despite their loss of appetite, survived the disease better than mice that restricted their caloric intake. What's more, in the well-fed mice, the salmonella strains actually got on board and began working to inhibit the body's appetite loss.
The bugs did so by producing a molecule called SlrP which keeps an immune protein known as a cyotikine from becoming active in the intestines. Cytokine normally signals the brain to reduce appetite during illness. When suppressed, the brain doesn't get the "stop eating" signal and appetite levels remain robust.
So why would a bacterial invader work to keep its host in a healthier state?
The researchers believe it has to do with virulence versus transmission.
"What we found was that appetite loss makes the Salmonella more virulent, perhaps because it needs to go beyond the intestines to find nutrients for itself," said Sheila Rao, a Salk research associate and the first author on the study. "This increased virulence kills its host too fast, which compromises the bacteria's ability to spread to new hosts. The tradeoff between transmission and virulence has not been appreciated before – it was previously thought that virulence and transmission were coupled."
Indeed, it was found that in the mice that kept their appetites and survived, Salmonella was released in their feces where it could spread to other animals. If the bugs killed their host, that opportunity wouldn't exist.
Co-author Janelle Ayres, assistant professor at the Salk Institute's Nomis Foundation Laboratories for Immunobiology and Microbial Pathogenesis, says that even though the same link between infection, cytokeines and appetite loss in humans exists as in mice, more research will be needed to tease out the link between food and disease fighting. Additionally, she says that the link will always be dependent on the infecting agent.
However, the researchers say that the work could lead to new ways to treat bacterial infections, including nutritional approaches that might replace or support antibiotics, which are already starting to fail in some cases.
The study has been published in the journal Cell.
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