Babies acquire their first gut microorganisms from their mothers, as they pass through the birth canal, and even more as they feed. Thus, the microbiome is not inherited genetically, but some parts of it are acquired from a parent. However, most of our gut metagenome and the metagenomes of other habitats—collectively known as the human microbiome—is acquired from the environment or from other humans. Therefore, in a sense, we largely acquire our microbiomes horizontally. The OTUs of the gut microbiome vary substantially from one person to another. Intriguingly, the metabolic capacities of individuals consuming similar diets is remarkably similar, even when the precise composition of bacteria mediating these functions is different. This suggests that viewing our microbiome as our extracellular genome, rather than simply as a collection of different microorganisms, could be a helpful approach for understanding our own biology.
Since much of our microbiome is acquired during our lifetime, microbiomes can also be transplanted from one individual to another. If a recipient’s microbiome is removed or depleted, it can be replaced with the microbiome of a donor. This typically establishes a richness and composition that is very similar to that of the microbiome of the donor. Microbiome transplants have been used to restore the microbiomes of individuals who suffer from infectious diarrhea because the infection has resulted in a loss of the protective effect of their healthy microbiomes. Ultimately, metagenomic analysis of microbiomes should enable the development of microbial therapeutics that can be used to seed new microbiomes, but, for now, fecal transplants can be used effectively to recolonize a gut microbiome.
Microbiome transplants are also a helpful tool in experimental metagenomics. As discussed in the chapter, one of the best known experiments with microbiomes was built on the initial observation that the bacterial species living in the guts of obese mice and humans are distinct from those living in the guts of nonobese mice and humans. Investigators transplanted bacteria from the gut of an obese mouse to the gut of non-obese mice, and the non-obese mice gained weight rapidly. Ultimately, the collective energy-mining ability of the microbiome from obese mice was shown to be less than from lean mice.
Similar studies have been performed by transplanting the gut microbiomes from healthy children and malnourished children into germ-free mice and then monitoring their nutritional statuses. These studies have shown that intractable, and often fatal, malnutrition can also be a disease of the microbiome.