Abstract
The nervous and immune systems influence each other, allowing animals to rapidly protect themselves from changes in their internal and external environment. However, the complex nature of these systems in mammals makes it difficult to determine how neuronal signaling influences the immune response. Here we show that serotonin, synthesized in Caenorhabditis elegans chemosensory neurons, modulates the immune response. Serotonin released from these cells acts, directly or indirectly, to regulate G-protein signaling in epithelial cells. Signaling in these cells is required for the immune response to infection by the natural pathogen Microbacterium nematophilum. Here we show that serotonin signaling suppresses the innate immune response and limits the rate of pathogen clearance. We show that C. elegans uses classical neurotransmitters to alter the immune response. Serotonin released from sensory neurons may function to modify the immune system in response to changes in the animal's external environment such as the availability, or quality, of food.
Highlights
The nervous and immune systems respond quickly and precisely to the presence of pathogenic microbes in an animal’s environment
We show that synthesis of the neurotransmitter serotonin, in sensory neurons exposed to the environment, alters susceptibility to infection with Microbacterium nematophilum
Unlike infection with Pseudomonas aeruginosa, where serotonin signaling is required for behavioral avoidance, here serotonin signaling suppresses the immune response by regulating a G-protein signaling pathway in epithelial cells
Summary
The nervous and immune systems respond quickly and precisely to the presence of pathogenic microbes in an animal’s environment. Whilst the immune system activates cellular defenses to recognize and eliminate pathogens, changes in neuronal signaling alter animal behavior to avoid these microbes. The free-living soil nematode Caenorhabditis elegans utilizes conserved signaling pathways to trigger behavioral and innate immune responses to infection by several natural and clinicallyrelevant pathogens provided as a food source [3]. Release of the insulin like neuropeptide INS-7 from neuronal dense core vesicles suppresses the C. elegans intestinal immune response triggered by infection with P. aeruginosa PA14 [4] and this pathway is utilized by the pathogen to suppress host immune defenses [10]. Several studies have implicated mammalian neuropeptides and peptide hormones in neuronal regulation of immunity (reviewed in [11]) suggesting that these relationships are conserved, and studies in C. elegans have identified neurons as important modifiers of the immune response. An octopamine receptor has been shown to regulate the C. elegans immune response [12], the function of neurotransmitters in C. elegans immunity remains unexplored
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