Abstract
During intestinal infection, microbes induce ROS by various mechanisms in C. elegans. ROS can have beneficial roles, acting as antimicrobials and as signaling molecules that activate cytoprotective pathways. Failure to maintain appropriate levels of ROS causes oxidative stress and cellular damage. This review uses the Damage Response Framework to interpret several recent observations on the relationships between infection, host response, and host damage, with a focus on mechanisms mediated by ROS. We propose a unifying hypothesis that ROS drive a collapse in proteostasis in infected C. elegans, which results in death during unresolved infection. Because the signaling pathways highlighted here are conserved in mammals, the mentioned and future studies can provide new tools of hypothesis generation in human health and disease.