Dietary κ-carrageenan facilitates gut microbiota-mediated intestinal inflammation

The inflammatory effects of carrageenan (CGN), a ubiquitous food additive, remains controversial. Gut microbiota and intestinal homeostasis may be a breakthrough in resolving this controversy. Here we show that, kappa-CGN did not cause significant inflammatory symptoms, but it did cause reduced bacteria-derived short-chain fatty acids (SCFAs) and decreased thickness of the mucus layer by altering microbiota composition. Administration of the pathogenic bacterium Citrobacter rodentium, further aggravated the inflammation and mucosal damage in the presence of kappa-CGN. Mucus layer degradation and altered SCFA levels could be reproduced by fecal transplantation from kappa-CGN-fed mice, but not from germ-free kappa-CGN-fed mice. These symptoms could be partially repaired by administering probiotics. Our results suggest that kappa-CGN may not be directly inflammatory, but it creates an environment that favors inflammation by perturbation of gut microbiota composition and then facilitates expansion of pathogens, and this effect may be partially reversed by the introduction of probiotics.

Automated summary

Research suggests that kappa-CGN may not directly cause inflammation, but rather creates an environment that promotes inflammation by altering gut microbiota composition, leading to a decrease in short-chain fatty acids and thinning of the mucus layer. In the presence of pathogenic bacteria, the inflammation and mucosal damage are aggravated. Fecal transplantation from kappa-CGN-fed mice can reproduce these symptoms, which can be partially reversed by administering probiotics.