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ZFIN ID: ZDB-PUB-170217-2
The enteric nervous system promotes intestinal health by constraining microbiota composition
Rolig, A.S., Mittge, E.K., Ganz, J., Troll, J.V., Melancon, E., Wiles, T.J., Alligood, K., Stephens, W.Z., Eisen, J.S., Guillemin, K.
Date: 2017
Source: PLoS Biology   15: e2000689 (Journal)
Registered Authors: Eisen, Judith S., Ganz, Julia, Guillemin, Karen, Mittge, Erika K.
Keywords: none
MeSH Terms:
  • Animals
  • Bacteria/growth & development
  • Bacteria/isolation & purification
  • Cell Count
  • Colony Count, Microbial
  • Dysbiosis/genetics
  • Dysbiosis/microbiology
  • Dysbiosis/pathology
  • Enteric Nervous System/cytology
  • Enteric Nervous System/physiology*
  • Gastrointestinal Microbiome*
  • Gene Expression Regulation
  • Inflammation/genetics
  • Inflammation/pathology
  • Intestines/microbiology*
  • Intestines/pathology
  • Leukocyte Count
  • Models, Biological
  • Mutation/genetics
  • Neutrophils/metabolism
  • Phylogeny
  • SOXE Transcription Factors/metabolism
  • Stem Cell Transplantation
  • Zebrafish
  • Zebrafish Proteins/metabolism
PubMed: 28207737 Full text @ PLoS Biol.
Sustaining a balanced intestinal microbial community is critical for maintaining intestinal health and preventing chronic inflammation. The gut is a highly dynamic environment, subject to periodic waves of peristaltic activity. We hypothesized that this dynamic environment is a prerequisite for a balanced microbial community and that the enteric nervous system (ENS), a chief regulator of physiological processes within the gut, profoundly influences gut microbiota composition. We found that zebrafish lacking an ENS due to a mutation in the Hirschsprung disease gene, sox10, develop microbiota-dependent inflammation that is transmissible between hosts. Profiling microbial communities across a spectrum of inflammatory phenotypes revealed that increased levels of inflammation were linked to an overabundance of pro-inflammatory bacterial lineages and a lack of anti-inflammatory bacterial lineages. Moreover, either administering a representative anti-inflammatory strain or restoring ENS function corrected the pathology. Thus, we demonstrate that the ENS modulates gut microbiota community membership to maintain intestinal health.