Intestinal infections can destabilise the connections between epithelial cells, causing the intestine to lose its protective barrier function, according to research conducted by scientists in Wrocław.
The study, titled "Impact of Isoquinoline Alkaloids on the Intestinal Barrier in a Colonic Model of Campylobacter jejuni Infection", was carried out by researchers from the Wrocław Medical University, Wrocław University of Science and Technology and University of Wrocław. The team examined how infection with Campylobacter jejuni affects the structure of the large intestine and whether berberine can modify this process.
According to a press release from Wrocław Medical University, intestinal infection is not solely the result of bacteria being present in the gastrointestinal tract. Campylobacter jejuni produces factors that directly affect intestinal epithelial cells, destabilising the junctions between them. These junctions are responsible for maintaining the tightness of the intestinal barrier and controlling what enters the body.
“Intestinal infections, including the most dangerous invasive ones, are associated not only with the presence of pathogenic bacteria but also with damage to the delicate intestinal lining, which is crucial for proper intestinal function,” said Anna Duda-Madej, PhD, MD, from the Department of Microbiology at Wrocław Medical University.
She explained that when this lining is damaged, the intestine loses its protective barrier function. Increased permeability allows bacterial antigens and inflammatory mediators to penetrate, potentially sustaining inflammation even after the pathogen has been eliminated.
In the experimental model used by the researchers, berberine demonstrated a dual effect. It limited the proliferation of Campylobacter jejuni and significantly reduced the bacterium’s ability to form biofilm, a structure that promotes survival and prolonged contact with the epithelium. At the same time, it showed a protective effect on intestinal cells by stabilising their connections and limiting the increase in barrier permeability.
“In our study, we have demonstrated that berberine overcomes both of these problematic situations simultaneously. This dual action is particularly important because even after the infection subsides, the barrier itself can remain weakened, contributing to prolonged symptoms,” Duda-Madej said.
The findings have potential clinical implications. Researchers emphasised that effectively responding to infection involves not only eliminating the microorganism but also restoring intestinal integrity. Persistent barrier dysfunction may explain why some patients continue to experience digestive symptoms long after campylobacteriosis has resolved.
“One reason for persistent symptoms may be the so-called leaky intestinal barrier, a condition that promotes permeability to bacterial antigens and inflammatory mediators,” Duda-Madej said.
By stabilising intercellular junctions, berberine may support the gradual reconstruction of the tight epithelial layer. The researchers noted that this does not constitute curing the infection in a pharmacological sense, but suggests a potential role in supporting intestinal regeneration and reducing long-term consequences.
“This study does not strictly confirm the clinical usefulness of berberine, but clearly demonstrates that the intestinal barrier should be considered a key element in recovery from intestinal infections, not merely a passive victim of infection,” the release stated. (PAP)
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