How Does a Stroke Disrupt the Gut’s “Good Bacteria”—And Why Does It Matter for Recovery?

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Healthcare (Commonwealth Union) – Gut health has for long periods considered a key factor for overall health.

Scientists at The University of Manchester have discovered new clues—based on experiments in mice—about why the gut’s immune system shifts after a stroke and how those changes may trigger digestive issues.

Appearing in Brain, Behaviour and Immunity, the research strengthens growing evidence for the “gut–brain axis,” a concept describing two-way communication between the brain and the digestive system in both normal function and illness.

The findings help clarify stroke biology. Stroke is a serious medical emergency caused by interrupted blood flow to parts of the brain, often leaving long-lasting impacts on movement and thinking.

People who experience a stroke face a heightened risk of secondary bacterial infections and frequently develop gastrointestinal symptoms such as trouble swallowing or constipation.

A growing body of research suggests that these digestive complications are linked to disruptions in the commensal microbiota—the beneficial community of bacteria that normally supports gut health.

Researchers have observed these changes in both people who experience strokes and in animal stroke models, yet the causes behind these gut-related issues—and their influence on how severe a stroke becomes or how well someone recovers—remain unclear.

Earlier work by some of the same scientists showed that signals from the nervous system can shift the gut’s immune activity after a stroke.

In this new study, supported by the Wellcome Trust, the researchers found that the communication between the gut and brain may operate in both directions. They discovered that antibody-producing immune cells can travel to the brain and its surrounding membranes during a stroke, though it is still uncertain how this movement affects stroke outcomes.

Using mice, the researchers examined what happened in the small intestine after a stroke and found that groups of immune cells responsible for producing antibodies underwent changes within the first few days.

 

 

They discovered that a specific group of cells responsible for producing the antibody Immunoglobulin A (IgA) became unusually active. IgA helps regulate the balance of the friendly bacteria living in the gut, which plays an important role in maintaining intestinal health.

The team also observed that mice unable to produce IgA did not show the same level of microbiome disruption after a stroke. This indicates that changes in immune activity may partly account for the alterations seen in the digestive system of stroke patients.

Professor Matt Hepworth, the lead author from the Lydia Becker Institute of Immunity and Inflammation at The University of Manchester, indicated that a stroke is a severe neurological incident that can trigger a range of lasting effects, leaving individuals more vulnerable to respiratory infections and digestive issues.

 

“Working with neuroscientists, we were able to begin to uncover how the immune system in the gut becomes disturbed following a stroke, and how that might lead to changes in the way the gut deals with its “good bacteria”.

 

“We now think these immune changes might contribute to the intestinal symptoms and long-term complications seen in stroke patients.”

 

Professor Hepworth further indicated that although preventing strokes and providing swift treatment to limit harm in those affected are still the main priorities, their findings shed new light on the wider bodily disorders that can develop afterward and may play a role in long-term problems during recovery.

He further added that with immune-focused treatments becoming more common in medical practice, there is growing potential to address immune-related symptoms that appear after a stroke, helping to enhance patients’ overall quality of life.

As stroke remain more frequent across the globe improvements and further research similar to what the researchers have found could play a crucial role in recovery.

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