Speaker
Claude Loverdo
Description
The body is home to a diverse microbiota, mainly in the gut. Using
stochastic models of bacterial population dynamics, we contributed to
show that the main physical effect of a type of antibodies which are the
main effector of the adaptive immune response secreted in the gut, is
to cross-link bacteria into clusters as they divide, preventing them from
interacting with epithelial cells, thus protecting the host. This yields
clonal clusters of bacteria, which could impact the diversity of the
bacterial population, and thus adaptation. Resistant bacteria are
selected for by antibiotic treatments, and once resistance becomes
widespread in a population of hosts, antibiotics become useless. Here,
we develop a multiscale model of the interaction between antibiotic use
and resistance spread in a host population, focusing on this important
aspect of within-host immunity. We demonstrate that immunity-driven
bacteria clustering can hinder the spread of a novel resistant bacterial
strain in a host population. We quantify this effect both in the case
where resistance pre-exists and in the case where acquiring a new
resistance mutation is necessary for the bacteria to spread. We further
show that the reduction of spread by clustering can be countered when
immune hosts are silent carriers, and are less likely to get treated,
and/or have more contacts. We demonstrate the robustness of our
findings to including stochastic within-host bacterial growth, a fitness
cost of resistance, and its compensation. Our results highlight the
importance of interactions between immunity and the spread of
antibiotic resistance, and argue in the favor of vaccine-based strategies
to combat antibiotic resistance.
Primary author
Claude Loverdo
