Research At The Salk Institute Suggests Simple Nutrient Support May Help Cure Infections

This is trying to. I'm Maureen Cavanaugh. Being hungry when you are sick is a physical response not feeling well and it's even been medical advice but a new study seems to indicate that not eating could make you sicker and make your disease more stronger and decrease your chance of survival. Joining me is Janelle Ayres a assistant professor at Salk Institute , Nomis Foundation Laboratories for Immunobiology and Microbial Pathogenesis. What made you want to focus on the last -- loss of appetite? It is well-known that when we suffer an infection, we suffer from what we call loss of appetite. We've been very interested for a long time in understanding what is the function of this loss of appetite if any for patients ability to survive an infectious disease. Previous studies including studies of my own have been designed in such a way that they been biased to only examine the patient is going to respond to last of dust loss of appetite but of course the patient's response is half of the host and equation. You wanted to initiate a study to look at how the pathogens respond to the loss of appetite and how it responds to nutritional interventions and how does that dictate the patient's outcome to the infection. Your study involved with mice did you find that the mice did lose their appetite when they got sick quick They do naturally lose their appetite. They are a great model system to study physiological responses during an infection that we reserve in humans -- observing humans. You found that the sick mice got sicker. Right. We infected these animals without oral pathogen called salmonella and it infects humans and what we found was that if the animals to develop this anorexic response that they did have a worse outcome during a salmonella infection. Then you gave them more nutrients how did that change how the disease progressed quick We found that when we provided nutritional intervention that the animals survived the infection. They had a better outcome with the infection. So the additional nutrients not only had a better outcome for the mice but changed the behavior of the bacteria quick Right. That is what was surprising to us is the prediction going in was that nutrients could optimize the ability to fight the infection. What we found was that wasn't the case. The reason why nutritional intervention promoted survival of the animals is because it tamed the behavior of the salmonella rather than invading beyond the small intestine and going into systemic tissues, it remained in the small intestine. So it is less dangerous infection to the animal. You make a different dance what the bacteria grows with within the body -- It is the ability to the pathogen to cause a disease. When we hear the here test the word bacteria it evokes very negative feelings and we think that all bacteria is out to get us. But what pathogens are evolving for is they are adapting to acquire stable nutrient supplies to replicate transmission. What we found was that in these animals where they were nutrient restricted and affected, the salmonella became more variant but we found that came with the cost to the transmission potential of the salmonella to do host. This was detrimental to the salmonella. You also found that the bacteria can interfere with the body's loss of appetite. In fact, it can promote a sense of appetite or try to interfere with that loss of appetite. Right. We found that there were trade-offs between the ability of the salmonella to cause disease and its transmission potential, that suggested that perhaps it has actually evolved ways in which it can block this response to become less very light and promote the transmission to new house. That is exactly what we found. We identified a gene and a mechanism by which salmonella can block the loss of appetite response during infection and by doing so it promoted survival of the host and also promoted transmission to new house. How did you find that the bacteria inhibited this anorexic response quite We think this is a really cool mechanism by which the salmonella does this. During infection, we found that there is activation of inflammatory response in the small intestine and that signals to a region in our brain that controls our appetite via a nerve. We found that it has actually evolved a way to block that immune response in the small intestine providing the signal to the nerve to the brain. Is a way to manipulate that brain circuitry. Have you think this study with mice might translate to humans? So I think there's huge translational potential with the study. We know loss of appetite occurs with many types of infectious diseases as well as noninfectious diseases in humans. And implication that I think is the suggest that perhaps there are simpler ways in which way we could treat infectious diseases. We know that our go to way for treating diseases is to prescribe antibiotics for patients that have bacterial infections and we are well aware of that antibiotic resistance crisis that we are in today. So if we can understand alternative means to promote health and survival of a patient when they are infected rather than antibiotics then we can over time this crisis. Is suggest that perhaps there are simpler ways to treat these diseases and provide nutritional interventions if we understand how the agent of the disease is going to respond to those interventions. That is fascinating. I have been speaking with Janelle Ayres he test -- thank you for having me.