Abstract
Intact intestinal barrier function is essential for maintaining intestinal homeostasis. A dysfunctional intestinal barrier can lead to local and systemic inflammation through translocation of luminal antigens and has been associated with a range of health disorders. Butyrate, a short-chain fatty acid derived from microbial fermentation of dietary fibers in the colon, has been described as an intestinal barrier-strengthening agent, although mainly by using in vitro and animal models. This study aimed to investigate butyrate’s ability to prevent intestinal hyperpermeability, induced by the mast cell degranulator Compound 48/80 (C48/80), in human colonic tissues. Colonic biopsies were collected from 16 healthy subjects and intestinal permeability was assessed by Ussing chamber experiments. Furthermore, the expression levels of tight junction-related proteins were determined by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Pre-treatment with 5 mM butyrate or 25 mM butyrate did not protect the colonic tissue against induced paracellular or transcellular hyperpermeability, measured by FITC-dextran and horseradish peroxidase passage, respectively. Biopsies treated with 25 mM butyrate prior to stimulation with C48/80 showed a reduced expression of claudin 1. In conclusion, this translational ex vivo study did not demonstrate an acute protective effect of butyrate against a chemical insult to the intestinal barrier in healthy humans.
Highlights
The intestine is the main organ involved in the uptake of nutrients and water
In humans, altered intestinal permeability has been associated with the pathogenesis of several gastrointestinal disorders including inflammatory bowel diseases (IBDs), irritable bowel syndrome (IBS) and celiac disease [3,4]
These diseases have been associated with low-grade systemic inflammation, gut microbiota dysbiosis and lower levels of butyrate-producing bacteria in the gut [8,9,10,11,12,13]
Summary
The intestine is the main organ involved in the uptake of nutrients and water. The intestinal barrier provides an essential separation between the intestinal lumen and the internal body environments and, thereby, between luminal antigens and the body’s immune system. A well-functioning intestinal barrier, thereby, allows the uptake of nutrients and simultaneously serves as an appropriate defense against the translocation of potentially harmful substances such as lipopolysaccharides (LPSs) or microorganisms that could trigger the immune system. The passage of these substances through a dysfunctional intestinal barrier may lead to local or systemic inflammation and have negative consequences for both intestinal and systemic health. These diseases have been associated with low-grade systemic inflammation, gut microbiota dysbiosis and lower levels of butyrate-producing bacteria in the gut [8,9,10,11,12,13]
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