@article{aaadafb4ee2c4d5da98abf1cdb94acea,
title = "Microbial Colonization Activates an Immune Fight-and-Flight Response via Neuroendocrine Signaling",
abstract = "The ability to distinguish harmful and beneficial microbes is critical for the survival of an organism. Here, we show that bloating of the intestinal lumen of Caenorhabditis elegans caused by microbial colonization elicits a microbial aversion behavior. Bloating of the intestinal lumen also activates a broad innate immune response, even in the absence of bacterial pathogens or live bacteria. Neuroendocrine pathway genes are upregulated by intestinal bloating and are required for microbial aversion behavior. We propose that microbial colonization and bloating of the intestine may be perceived as a danger signal that activates an immune fight-and-flight response. These results reveal how inputs from the intestine can aid in the recognition of a broad range of microbes and modulate host behavior via neuroendocrine signaling. Singh and Aballay describe a mechanism by which a fight-and-flight response against pathogenic microbes is activated. They show that in C. elegans microbial colonization induces bloating of the intestinal lumen, which enhances the expression of innate immune genes and neuroendocrine pathway genes required for the elicitation of a microbial aversion behavior.",
keywords = "C. elegans, daf-7, defecation motor program, eat-2, innate immunity, microbial colonization, neuroendocrine, npr-1, pathogen avoidance behavior, unc-25",
author = "Jogender Singh and Alejandro Aballay",
note = "Funding Information: This work was supported by NIH grants GM0709077 and AI117911 (to A.A.). Some strains used in this study were provided by the Caenorhabditis Genetics Center (CGC), which is funded by the NIH Office of Research Infrastructure Programs ( P40 OD010440 ). We thank Javier E. Irazoqui (University of Massachusetts Medical School, Worcester, MA 01605) for providing the clec-60p::GFP strain and Meta Kuehn (Duke University Medical Center, Durham, NC) for providing the P. aeruginosa gacA mutant. We are also grateful for the critiques and comments of the reviewers that improved our manuscript. Funding Information: This work was supported by NIH grants GM0709077 and AI117911 (to A.A.). Some strains used in this study were provided by the Caenorhabditis Genetics Center (CGC), which is funded by the NIH Office of Research Infrastructure Programs (P40 OD010440). We thank Javier E. Irazoqui (University of Massachusetts Medical School, Worcester, MA 01605) for providing the clec-60p::GFP strain and Meta Kuehn (Duke University Medical Center, Durham, NC) for providing the P. aeruginosa gacA mutant. We are also grateful for the critiques and comments of the reviewers that improved our manuscript. J.S. and A.A. conceived and designed the experiments. J.S. performed the experiments. J.S. and A.A. analyzed the data and wrote the paper. The authors declare no competing interests. Publisher Copyright: {\textcopyright} 2019 Elsevier Inc.",
year = "2019",
month = apr,
day = "8",
doi = "10.1016/j.devcel.2019.02.001",
language = "English (US)",
volume = "49",
pages = "89--99.e4",
journal = "Developmental Cell",
issn = "1534-5807",
publisher = "Cell Press",
number = "1",
}