In recent years, new research programmes have been initiated to understand the role of gut bacteria in health and disease, enabled in large part by the emergence of high-throughput sequencing. As new genomic and other data emerge it will become important to explain observations in terms of underlying population mechanisms; for instance, it is of interest to understand how resident bacteria interact with their hosts and pathogens, and how they play a protective role. Connecting underlying processes with observed patterns is aided by the development of mathematical models. Here, we develop a spatial model of microbial populations in the gastrointestinal tract to explore conditions under which inflammation-causing bacteria can invade the gut and under which such pathogens become persistent. We find that pathogens invade both small and large intestine from even a relatively small inoculum size but are usually eliminated by the host response. When the immune response is weak, the pathogen is able to persist for a long period. Spatial structure affects these dynamics by creating moving refugia which facilitate bouts of pathogen resurgence and inflammation in persistent infections. Space also plays a role in repopulation by commensals after infection. We further find that the rate of decay of inflammation has a stronger effect on outcomes than the initiation of inflammation or other parameters. Finally, we explore the impact of partially inflammation-resistant commensals on these dynamics.
Keywords: Gut bacteria; Inflammation; Mathematical model; Microbiota; Pathogen; Recolonisation; Spatial structure.
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