Evolutionary and ecological forces that shape the bacterial communities of the human gut

Abstract

Since microbes were first described in the mid-1600s, we have come to appreciate that they live all around and within us with both beneficial and detrimental effects on nearly every aspect of our lives. The human gastrointestinal tract is inhabited by a dynamic community of trillions of bacteria that constantly interact with each other and their human host. The acquisition of these bacteria is not stochastic but determined by circumstance (environment), host rules (genetics, immune state, mucus, etc), and dynamic self-selection among microbes to form stable, resilient communities that are in balance with the host. In this review, we will discuss how these factors lead to formation of the gut bacterial community and influence its interactions with the host. We will also address how gut bacteria contribute to disease and how they could potentially be targeted to prevent and treat a variety of human ailments.

Figure 1. Metabolic cross feeding during gut colonization

Fructooligosaccharides (FOS) reach the colon largely intact where they serve as substrates for fructan-degrading bacteria such as Bifidobacteria. Utilization of down-stream products by other bacterial species, termed metabolic cross-feeding, results in production of short-chain fatty acids that are absorbed by the host. Strain variation in FOS-degradative capacity results in diet-dependent colonization or replicative capacity.

Figure 2. Bacterial strategies to evade host defenses

A) Addition of phosphorylcholine (CHOP) to bacterial lipooligosaccharide (LOS) reduces surface electronegativity and thus resistance to cationic peptides. B) Secretory IgA (sIgA) immune complexes promote M cell uptake of commensal microbial antigen. Induction of this pathway is important for induction of host-commensal homeostasis. C) Capsular polysaccharide A (PSA) from Bacteroides fragilis induces an IL-10 predominant immune response. This, in turn, is associated with protection from mucosal damage in murine models of colitis.