Introduction  Human microbiota-associated (HMA) models are used to allow in vivo studies of the human gut microbiome and its effects on host physiology. In particular, alterations in early life microbiota have been linked to allergy development during childhood. In this study, we investigated how pools of human microbiota collected from infants with different allergy risk, thrive in mice and their offspring, as well as how they influence the host metabolome.

Method  We used a two-generation HMA mouse model in which dams were colonized with human feces from three groups of infants (n = 19, samples collected during the first 8 weeks of life). In two of the groups, all infants had a strong hereditary risk for allergic disease (n = 12), but only 6 of them developed allergy before 2 years of age. In the third group, which was used as a control, none of the infants had allergic heredity or developed allergy (n = 7). Microbiota trajectories were followed from inoculation to mouse offspring, and metabolic profiles were monitored in several intestinal organs as well as in the serum of the murine offspring.

Results  The human microbiota adapted to the murine host but still presented distinct compositional features, reflecting the original inoculated samples. These microbial differences were mirrored in the mouse offspring metabolome, with group-associated patterns in sphingolipids, acylcarnitines and tryptophan metabolites. Furthermore, the metabolic profiles of the mouse offspring aligned with those observed in fecal water preparations from the corresponding human infant fecal samples.

Conclusion  Our findings highlight the significant impact of early-life microbiota on the host metabolome and show that our two-generation HMA model is suitable for studying microbiota‒metabolome relationships relevant to humans. The differences in microbiota‒metabolome correlations between individuals who develop or do not develop allergic disease suggest that an allergic predisposition might be more multifaceted than previously believed.

In aquatic ecosystems, microplastics are a relatively new anthropogenic substrate that can readily be colonized by biofilm-forming organisms. To examine the effects of substrate type on microbial community assembly, we exposed ambient Baltic bacterioplankton to plastic substrates commonly found in marine environments (polyethylene, polypropylene and polystyrene) as well as native (cellulose) and inert (glass beads) particles for 2 weeks under controlled conditions. The source microbial communities and those of the biofilms were analyzed by Illumina sequencing of the 16S rRNA gene libraries. All biofilm communities displayed lower diversity and evenness compared with the source community, suggesting substrate-driven selection. Moreover, the plastics-associated communities were distinctly different from those on the non-plastic substrates. Whereas plastics hosted greater than twofold higher abundance of Burkholderiales, the non-plastic substrates had a significantly higher proportion of Actinobacteria and Cytophagia. Variation in the community structure, but not the cell abundance, across the treatments was strongly linked to the substrate hydrophobicity. Thus, microplastics host distinct bacterial communities, at least during early successional stages.

The intestinal microbiota influences immune maturation during childhood, and is implicated in early-life allergy development. However, to directly study intestinal microbes and gut immune responses in infants is difficult. To investigate how different types of early-life gut microbiota affect immune development, we collected fecal samples from children with different allergic heredity (AH) and inoculated germ-free mice. Immune responses and microbiota composition were evaluated in the offspring of these mice. Microbial composition in the small intestine, the cecum and the colon were determined by 16S rRNA sequencing. The intestinal microbiota differed markedly between the groups of mice, but only exposure to microbiota associated with AH and known future allergy in children resulted in a T helper 17 (Th17)-signature, both systemically and in the gut mucosa in the mouse offspring. These Th17 responses could be signs of a particular microbiota and a shift in immune development, ultimately resulting in an increased risk of allergy.