Brain-wide imaging in flp-13 animals upon PA14 infection

When animals are infected by a pathogen, peripheral sensors of infection
signal to the brain to coordinate a set of adaptive behavioral changes
known as sickness behaviors. While the pathways that signal from the
periphery to the brain have been intensively studied in recent years, how
central circuits are reconfigured to elicit these behavioral changes is
not well understood. Here, we find that neuromodulatory systems linked to
stress and satiety are recruited during chronic pathogen infection to
alter the behavior of C. elegans. Upon chronic infection by the bacterium
Pseudomonas aeruginosa PA14, C. elegans decrease their feeding behavior,
then display reversible bouts of quiescence, and eventually die. The ALA
neuron and its neuropeptides FLP-7, FLP-24, and NLP-8, which control
stress-induced sleep in uninfected animals, promote the PA14-induced
feeding reduction. However, the ALA neuropeptide FLP-13 instead acts to
delay quiescence and death in infected animals. Cell-specific genetic
perturbations show that the neurons that release FLP-13 to delay
quiescence in infected animals are distinct from ALA. A brain-wide imaging
screen reveals that infection-induced quiescence involves ASI and
DAF-7/TGF-beta, which control satiety-induced quiescence in uninfected
animals. Our results suggest that a common set of neuromodulators are
recruited across different physiological states, acting from distinct
neural sources and in distinct combinations to drive state-dependent
behaviors.