Editorial: Mechanisms of fermented foods and interactions with the gut microbiome

Fermentation has shaped human diets for millennia, valued first as a means of preserving food and later for enhancing the organoleptic properties of foodstuffs. Only in recent years, however, have we started to understand how fermentation actively reshapes the biological properties of fermented food matrices. Across cultures, fermented foods such as kefir, sauerkraut, and fermented legumes have long been dietary staples, yet how they influence host physiology has not been fully understood. Some of the primary benefits of fermentation come from its transformation of the food matrix to generate new metabolites and, in many cases, from the introduction of beneficial, live microorganisms capable of interacting directly with the gut. This Research Topic, Mechanisms of Fermented Foods and Interactions with the Gut Microbiome, brings together ten contributions-eight research papers and two reviews-that examine these interactions from several angles: how specific fermented foods alter gut microbial composition, how fermentation-derived microbes and metabolites act on distant organs through gut-mediated axes, and how the fermentation process itself determines a food's downstream interaction with the gut. Together, they build a mechanistic picture of why fermented foods matter for gut health, rather than a purely associative one, marking a substantial contribution to a growing body of mechanistic fermented-food research.Two contributions opened this evidence base with human trials that isolate fermented dairy as the variable of interest. Ní Chonnacháin et al. found that unmelted Cheddar cheese increased faecal bacterial diversity in a controlled six-week trial, while an equivalent melted-cheese arm did not, with Dorea, Erysipelotrichaceae UCG-003, and Bacteroides shifting specifically in the unmelted groupevidence that processing state, not fermentation alone, shapes a dairy food's microbial effect. Through a randomized, controlled, parallel-group trial, Choi et al. showed that two weeks of kefir consumption (daily 150 mL) in healthy participants aged 18-30 years increased the abundance of lactate-producing taxa, including Bifidobacterium breve, Ruthenibacterium lactatiformans, Weissella koreensis, and Leuconostoc mesenteroides, along with Blautia species, distinguishing kefir's microbial signature from both unfermented milk and yogurt comparators. Together, these studies establish that even within a single category, fermentation's gut effects depend on how the food is made and 47 consumed. 48A second cluster of contributions moves beyond compositional change to trace 49 mechanistic pathways from fermented-food microbes to organs well beyond the gut. the gut-brain axis across models of autism, depression, and neurodegeneration, in addition to their 65 potential benefits for immune homoeostasis and the management of chronic diseases, including IBD. 66 Across all three, the through-line is the same: a defined microbe or metabolite, traceable to a 67 fermented food, acting on a specific organ system via the gut. 68A third pair of contributions examined fermented foods through a gut-liver lens, using high-fat diet 69 mouse models to connect microbial shifts to systemic lipid handling. with phytosterol and lycopene and found that the combination lowered LDL cholesterol more 78 effectively than simvastatin in hypercholesterolaemic mice, although the benefit was dose-dependent 79 and warrants further study, while also reducing body weight, an effect the statin did not produce; the 80 mechanism traced back to a shift toward Bifidobacterium and away from Clostridium and 81Ruminococcus, altering the bile-acid pool in a way that activated the hepatic FXR pathway and 82 increased faecal cholesterol excretion. In both cases, fermentation-associated microbial change 83precedes and appears to drive the metabolic outcome, rather than merely accompanying it. 84 Three further contributions shift the focus from finished fermented foods to the mechanism of 85 fermentation itself -why processing a food changes its relationship with the gut before it is even 86 consumed. The review by Panapparambil Sooraj et al. argues that plant proteins, with their lower 87 digestibility and anti-nutritional factors, leave more undigested protein to reach the colon, where 88 bacterial putrefaction generates ammonia, phenols, and other by-products linked to inflammation 89 and gut barrier dysfunction; fermentation degrades those anti-nutritional factors and increases free 90 amino acids, reducing the undigested protein load before it can be putrefied. Therefore, fermentation 91 could be considered a potential way to improve the digestibility of plant proteins and reduce the risk 92 of putrefaction. Yang et al. showed a parallel effect on a plant substrate's chemistry rather than its 93 protein content: fermenting honeysuckle liquid with Lactobacillus acidophilus raised total phenols (by 94 26.48%), flavonoids and chlorogenic acid (33.57%) well above unfermented levels, along 95 with antioxidant and alpha-glucosidase-inhibitory activity. This study showed that Lactobacillus 96 acidophilus fermentation could be a potential approach for developing honeysuckle functional 97 products. Rounding out this group, Aziz et al. providedthe first genomic characterisation of a 98 sauerkraut-derived Lactiplantibacillus plantarum strain, HMX2, mapping bacteriocin genes and stress-99 survival genes relevant to its candidacy as a functional probiotic -foundational work for the kind of 100 strain-level claims made elsewhere in this Research Topic. 101Taken together, the ten contributions to this Research Topic contribute to the field's continuing, 102 gradual shift from association toward mechanism. Two studies show even a single 103 fermented food, its form and how it is consumed can determine its effect on the gut. Three further 104 studies trace specific microbes or metabolites along defined axes connecting the gut to the lung, the 105 colon's own barrier, and the brain. Two more studies show that fermentation-derived microbial and 106 bile-acid shifts can outperform a standard pharmaceutical on some metabolic endpoints, and two 107 further studies, together with a foundational genomic characterisation, explain why fermentation 108 changes a food's gut-interaction potential before it is even eaten. What remains is the harder 109 translational step: converting these strain-and metabolite-level mechanisms into dietary guidance 110 and functional-food design. This will require more controlled human trials of the kind reported here, 111 rather than relying solely on further animal-model evidence. We hope this collection offers a 112 foundation for that next phase of fermented-food research, an area now entering an exciting period 113 of discovery and innovation.