PUBLICATION

The enteric nervous system promotes intestinal health by constraining microbiota composition

Authors
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.
ID
ZDB-PUB-170217-2
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.
Abstract
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.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping