Host-to-host variation of ecological interactions in polymicrobial infections

TL;DR

This study investigates how interactions among bacteria in polymicrobial infections vary between hosts, revealing that these variations are influenced by bacterial interactions and immune responses, which may drive coevolution.

Contribution

It introduces a mechanistic approach combining population models and MaxEnt inference to analyze host-to-host variability in microbial interactions during infections.

Findings

Bacterial interactions critically influence host-to-host variation.

Unrelated phenomena like nutrient utilization and immune response become interdependent.

Potential mechanism for strain selection during host-microbe coevolution.

Abstract

Host-to-host variability with respect to interactions between microorganisms and multicellular hosts are commonly observed in infection and in homeostasis. However, the majority of mechanistic models used in analyzing host-microorganism relationships, as well as most of the ecological theories proposed to explain co-evolution of host and microbes, are based on averages across a host population. By assuming that observed variations are random and independent, these models overlook the role of inter-host differences. Here we analyze mechanisms underlying host-to-host variations, using the well-characterized experimental infection model of polymicrobial otitis media (OM) in chinchillas, in combination with population dynamic models and a Maximum Entropy (MaxEnt) based inference scheme. We find that the nature of the interactions among bacterial species critically regulates host-to-host variations of these interactions. Surprisingly, seemingly unrelated phenomena, such as the efficiency of individual bacterial species in utilizing nutrients for growth and the microbe-specific host immune response, can become interdependent in a host population. The latter finding suggests a potential mechanism that could lead to selection of specific strains of bacterial species during the coevolution of the host immune response and the bacterial species.