Humans and their gut microbiota have co-evolved over thousands of years, resulting in the establishment of a complex host-microbiota ecosystem. Early life environmental factors, such as delivery mode, nutrition, and medication use, have been shown to substantially affect both host-microbiota interactions and health outcomes. However, the effects of urbanization (characterized by the spectrum of rural and urban populations) on these early life events have been overlooked. A deeper understanding of the relationship between urbanization and microbiota development will allow for the identification of novel biological and social approaches that can be implemented to prevent and treat disease and promote maternal and infant/child health. The aim of this narrative review is to summarize how factors associated with urbanization differentially impact delivery mode, nutrition, and medication use, and how these changes subsequently affect the gut microbiota and health outcomes of infants. This narrative review also describes the important evidence gaps associated with these relationships and recommends actions that can be taken to improve the health of mothers and infants worldwide.

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Background The opportunistic pathogen Staphylococcus aureus is an asymptomatically carried member of the microbiome of about one third of the human population at any given point in time. Body sites known to harbor S. aureus are the skin, nasopharynx, and gut. In particular, the mechanisms allowing S. aureus to pass the gut epithelial barrier and to invade the bloodstream were so far poorly understood. Therefore, the objective of our present study was to investigate the extent to which genetic differences between enteric S. aureus isolates and isolates that caused serious bloodstream infections contribute to the likelihood of invasive disease. Results Here, we present genome-wide association studies (GWAS) that compare the genome sequences of 69 S. aureus isolates from enteric carriage by healthy volunteers and 95 isolates from bloodstream infections. We complement our GWAS results with a detailed characterization of the cellular and extracellular proteomes of the representative gut and bloodstream isolates, and by assaying the virulence of these isolates with infection models based on human gut epithelial cells, human blood cells, and a small animal infection model. Intriguingly, our results show that enteric and bloodstream isolates with the same sequence type (ST1 or ST5) are very similar to each other at the genomic and proteomic levels. Nonetheless, bloodstream isolates are not necessarily associated with an invasive profile. Furthermore, we show that the main decisive factor preventing infection of gut epithelial cells in vitro is the presence of a tight barrier. Conclusions Our data show that virulence is a highly variable trait, even within a single clone. Importantly, however, there is no evidence that blood stream isolates possess a higher virulence potential than those from the enteric carriage. In fact, some gut isolates from healthy carriers were more virulent than bloodstream isolates. Based on our present observations, we propose that the integrity of the gut epithelial layer, rather than the pathogenic potential of the investigated enteric S. aureus isolates, determines whether staphylococci from the gut microbiome will become invasive pathogens.