Radioprotective bacteria: A common symptom of radiation treatment for cancer is gastrointestinal disruption. The damage caused can become so severe and debilitating that it interrupts treatment. Guo et al. noticed that mice surviving experimental radiation exposure had distinctive taxonomic representation in their gut microbiota. A similar correlation was also observed in a small group of human subjects. Further experiments in mice revealed that some strains of bacteria produced high levels of short-chain fatty acids, which seemed to be dampening inflammatory responses and alleviating the damage caused by reactive oxygen species released by the radiation. A metabolomics analysis also implicated a role for tryptophan metabolic pathways in radiation survivorship. Science , this issue p. eaay9097

Sucralose is the most widely used artificial sweetener and its health effects have been highly debated over the years. In particular, previous studies support that sucralose consumption could alter the gut microbiota. The gut microbiome plays a key role in host health, such as digestion and fermentation of food, development of immune cells, and regulation of the enteric nervous system. Inflammation is one of the most common physical conditions associated with the dysbiosis of the gut microbiome, which is linked to a series of human diseases, such as diabetes and obesity. The aim of this study is to investigate the structural and functional effects of sucralose on the gut microbiota and associated inflammation in the host. In this study, C57BL/6 male mice received sucralose in drinking water for six months. Difference in the gut microbiota and metabolites between controls and sucralose-treated mice was determined using 16S rRNA gene sequencing, functional gene enrichment analysis and metabolomics; Expression of inflammatory genes in tissues was determined with RT-PCR. Alterations of bacterial genera showed that sucralose affects the gut microbiota and its dynamics of development. Enrichment of bacterial genes of pro-inflammatory mediators and fecal metabolites suggest that sucralose consumption may increase the risk of developing tissue inflammation via disrupting the gut microbiota, which is consistent with elevated pro-inflammatory gene expression in liver of sucralose-treated mice. Our results highlight the role of sucralose-gut microbiome interaction in regulating host health, particularly chronic inflammation.

Artificial sweeteners have been widely used in the modern diet, and their observed effects on human health have been inconsistent, with both beneficial and adverse outcomes reported. Obesity and type 2 diabetes have dramatically increased in the U.S. and other countries over the last two decades. Numerous studies have indicated an important role of the gut microbiome in body weight control and glucose metabolism and regulation. Interestingly, the artificial sweetener saccharin could alter gut microbiota and induce glucose intolerance, raising questions about the contribution of artificial sweeteners to the global epidemic of obesity and diabetes. Acesulfame-potassium (Ace-K), a FDA-approved artificial sweetener, is commonly used, but its toxicity data reported to date are considered inadequate. In particular, the functional impact of Ace-K on the gut microbiome is largely unknown. In this study, we explored the effects of Ace-K on the gut microbiome and the changes in fecal metabolic profiles using 16S rRNA sequencing and gas chromatography-mass spectrometry (GC-MS) metabolomics. We found that Ace-K consumption perturbed the gut microbiome of CD-1 mice after a 4-week treatment. The observed body weight gain, shifts in the gut bacterial community composition, enrichment of functional bacterial genes related to energy metabolism, and fecal metabolomic changes were highly gender-specific, with differential effects observed for males and females. In particular, ace-K increased body weight gain of male but not female mice. Collectively, our results may provide a novel understanding of the interaction between artificial sweeteners and the gut microbiome, as well as the potential role of this interaction in the development of obesity and the associated chronic inflammation.

The mammalian gut harbors a complex and dynamic microbial ecosystem: the microbiota. While emerging studies support that microbiota regulates brain function with a few molecular cues suggested, the overall biochemical landscape of the “microbiota-gut-brain axis” remains largely unclear. Here we use high-coverage metabolomics to comparatively profile feces, blood sera, and cerebral cortical brain tissues of germ-free C57BL/6 mice and their age-matched conventionally raised counterparts. Results revealed for all three matrices metabolomic signatures owing to microbiota, yielding hundreds of identified metabolites including 533 altered for feces, 231 for sera, and 58 for brain with numerous significantly enriched pathways involving aromatic amino acids and neurotransmitters. Multicompartmental comparative analyses single out microbiota-derived metabolites potentially implicated in interorgan transport and the gut-brain axis, as exemplified by indoxyl sulfate and trimethylamine-N-oxide. Gender-specific characteristics of these landscapes are discussed. Our findings may be valuable for future research probing microbial influences on host metabolism and gut-brain communication.