  The body is home to a diverse microbiota, mainly in the gut. 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 an important aspect of
within-host immunity. Antibodies secreted in the gut enchain bacteria upon
division, yielding clonal clusters of bacteria. 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.
