Gut infection may train immune sentries at the brain's border to remember microbes
The brain and spinal cord are highly protected treasures of the central nervous system, wrapped under three protective layers of meninges. The outermost layer, the dura mater, has leaky windows through which bacteria or parasites ...
A recent study explored this question by conducting experiments in mice and exposing their intestines to several types of immune challenges, such as parasites, chemical gut irritants, and Salmonella infection. The findings are published in Nature Neuroscience.
They saw that upon encountering irritants, CD4+ T cells, white blood cells responsible for coordinating the battle against invaders, become activated and adapt specifically to fight that exact type of threat they are facing.
These highly specific T cells then find their way to the dura mater through a specialized chemical homing pathway. Once there, they remain for the long term, building immune memory around the region's blood vessels to help fight future infections and inflammation.
Elusive gut-brain link
The gut is a major source of microbes that can enter the bloodstream via fenestrated endothelium, a type of capillary structure that contains small pores. At the same time, immune cells in the dura mater stand ready to defend the brain's borders against these foreign entities, with inflammatory signals that can influence brain activity.
Scientists have known for a while that gut inflammation can be linked to brain-related symptoms and conditions. For instance, people who have inflammatory bowel disease (IBD) are known to experience higher rates of depression and anxiety.
In mice, gut infections send helper T cells to the dura, the outer brain covering to protect the brain borders. Credit: Pexels.
Researchers introduced dextran sodium sulfate (DSS) in a mouse's drinking water to model inflammatory bowel disease. Credit: Nature Neuroscience (2026). DOI: 10.1038/s41593-026-02428-4
Representative flow cytometry plots (left) or the quantification (right) of percentage of 2W1S antigen-specific CD4+ T cells in the specified organs post infection with bacteria. Credit: Nature Neuroscience (2026). DOI: 10.1038/s41593-026-02428-4