Signed: Nadine Yehya
A new study from UC Davis Health reveals how salmonella, a leading cause of food poisoning, can invade the gut even when protective bacteria are present. The study, published in the Proceedings of the National Academy of Sciences, explains how pathogens trick the gut environment to evade the body’s natural defenses.
Your digestive system is home to trillions of bacteria, many of which produce short-chain fatty acids (SCFAs) that help fight harmful pathogens. However, despite the presence of these protective compounds, Salmonella still manages to grow and spread in the intestines. This study asks: How does Salmonella evade this defense?
“We knew that Salmonella entered the small intestine, but the small intestine was not the main site of replication; the colon was,” said Andreas Baumler, lead author of the study. Baumler is a professor emeritus and associate research director in the Department of Medical Microbiology and Immunology at the University of California, Davis.
Baumler and his team found that the answer lies in how pathogens alter the nutritional balance of the gut. When Salmonella enters the small intestine, it causes inflammation of the intestinal lining and interferes with the normal absorption of amino acids from food. This will disrupt the balance of nutrients in your intestines.
This imbalance gives Salmonella the resources it needs to survive and multiply in the large intestine (colon), but friendly bacteria normally inhibit its growth. This study showed that Salmonella causes inflammation in the small intestine to obtain nutrients that promote replication in the colon.
Salmonella changes the nutritional environment in the intestine to survive
The research team used a mouse model to take a closer look at how Salmonella alters the chemical composition of the intestine. They tracked the absorption of amino acids in the small and large intestines.
They found that mice infected with Salmonella had reduced absorption of amino acids into the blood. In fact, two amino acids, lysine and ornithine, became more abundant in the intestine after infection. These amino acids prevented the growth-inhibitory effects of SCFAs and aided Salmonella survival. They achieved this by restoring the acidity (pH) balance of Salmonella, allowing the pathogen to evade the microbiome’s defenses.
“Our findings show that Salmonella has a clever way of altering the intestinal nutritional environment to its advantage. By making it difficult for the body to absorb amino acids in the ileum, Salmonella It creates a more favorable environment,” Baumler said.
The researchers showed that Salmonella uses its own virulence factors (disease-causing molecules) to activate enzymes that break down key amino acids such as lysine. This allows pathogens to evade the protective effects of SCFA and multiply more easily in the intestine.
New insights could lead to better intestinal infection treatments
New insights may explain how the intestinal environment changes during inflammatory bowel diseases such as Crohn’s disease and ulcerative colitis, and could lead to better treatments for intestinal infections There is. By understanding how Salmonella alters the gut environment, researchers hope to develop new ways to protect the gut microbiome and prevent these infections.
“This study uses a more holistic approach to studying gut health. This study not only provides a deeper understanding of how Salmonella acts, but also supports healthy gut bacteria. “This highlights the importance of maintaining the plexus,” said Lauren Radlinski, lead author of the study and a postdoctoral fellow at the Baumler Institute. “Our findings could lead to new treatments that help support the microbiome during infections.”
The findings could inspire future treatments, such as probiotics and dietary plans designed to strengthen the body’s natural defenses against harmful pathogens.
“By learning how pathogens manipulate host systems, we can discover ways to enhance the host’s natural defenses,” Radlinski said.
Co-authors of the study are Andrew Rogers, Lalita Bechtold, Hugo Masson, Henry Nguyen, Anaïs B. Larabi, Connor Tiffany, Thaynara Parente de Carvalho, and Renee Tsolis of UC Davis.
This research was supported by a Kenneth Rainin Foundation Award (20230029) and National Institutes of Health grants (AI169649, AI044170, AI096528, AI112445, AI112949 and DK138912).
