Host-microbe interactions and the behavior of Caenorhabditis elegans

Abstract

Microbes are ubiquitous in the natural environment of Caenorhabditis elegans. Bacteria serve as a food source for C. elegans but may also cause infection in the nematode host. The sensory nervous system of C. elegans detects diverse microbial molecules, ranging from metabolites produced by broad classes of bacteria to molecules synthesized by specific strains of bacteria. Innate recognition through chemosensation of bacterial metabolites or mechanosensation of bacteria can induce immediate behavioral responses. The ingestion of nutritive or pathogenic bacteria can modulate internal states that underlie long-lasting behavioral changes. Ingestion of nutritive bacteria leads to learned attraction and exploitation of the bacterial food source. Infection, which is accompanied by activation of innate immunity, stress responses, and host damage, leads to the development of aversive behavior. The integration of a multitude of microbial sensory cues in the environment is shaped by experience and context. Genetic, chemical, and neuronal studies of C. elegans behavior in the presence of bacteria have defined neural circuits and neuromodulatory systems that shape innate and learned behavioral responses to microbial cues. These studies have revealed the profound influence that host-microbe interactions have in governing the behavior of this simple animal host.

Keywords:

• Host-microbe interactions
• behavior
• C. elegans
• neuromodulator
• neuroimmune
• gut-brain
• neural circuits

Acknowledgements

We are grateful to the editors for the opportunity to write in honor of the memories of Sydney Brenner and John Sulston, who had central roles in the development of Caenorhabditis elegans as a simple organism for the molecular genetic analysis of behavior. We thank members of our research groups over the years who have joined us in studying host-microbe interactions of C. elegans.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

D.H.K. acknowledges funding from NIH GM084477. S.W.F acknowledges funding from NIH NS104892.