An edible seaweed-derived rhamnan sulfate modulates gut microbiota by promoting Mucispirillum schaedleri through bacterial interactions and enhancing anti-inflammatory and pathogen-protection mechanisms in mice

Gut microbiota plays crucial roles in host physiology and pathology throughout life. With the potential to harness the microbiota for improved health, various substances have been explored for their beneficial microbiota-modulating effects. We previously demonstrated that rhamnan sulfate (RS) from the seaweed Monostroma nitidum suppresses lipopolysaccharide-induced inflammation in mice. Although the mechanisms underlying the anti-inflammatory effect of RS remain unclear, it is plausible that the anti-inflammatory effects of RS are mediated by the modulatory effect of RS on the gut microbiota. In this study, we analyzed the gut microbiota of mice before and after oral RS administration. RS significantly altered the gut microbiota composition, increasing the abundances of Prevotellaceae UCG-001 , Clostridia vadinBB60 group , and Mucispirillum schaedleri —the sole species in the genus Mucispirillum —while decreasing those of Rikenellaceae RC9 gut group , ASF356 , and the pathogen Staphylococcus . M. schaedleri is known to thrive in inflammatory environments, scavenging oxygen and reactive oxygen species during inflammation. Functional analyses of microbial genomes demonstrated that RS altered the microbial communities, including shifts toward anti-inflammatory and anti-pathogen profiles. RS also elevated fecal acetic acid concentrations while tending to suppress bile acid production. Interestingly, M. schaedleri has a limited capacity for degrading complex polysaccharides, suggesting that RS is metabolized by other gut bacteria, creating nutrient niches that support M. schaedleri . These results suggest that RS fosters specific bacterial interactions that enhance M . schaedleri proliferation as a prebiotic , which likely contributes to the anti-inflammatory properties of RS and highlights the therapeutic potential of RS through gut microbiota modulation.