R-Spondin1 expands Paneth cells and prevents dysbiosis induced by graft-versus-host disease

J Exp Med. 2017 Dec 4;214(12):3507-3518. doi: 10.1084/jem.20170418. Epub 2017 Oct 24.

Abstract

The intestinal microbial ecosystem is actively regulated by Paneth cell-derived antimicrobial peptides such as α-defensins. Various disorders, including graft-versus-host disease (GVHD), disrupt Paneth cell functions, resulting in unfavorably altered intestinal microbiota (dysbiosis), which further accelerates the underlying diseases. Current strategies to restore the gut ecosystem are bacteriotherapy such as fecal microbiota transplantation and probiotics, and no physiological approach has been developed so far. In this study, we demonstrate a novel approach to restore gut microbial ecology by Wnt agonist R-Spondin1 (R-Spo1) or recombinant α-defensin in mice. R-Spo1 stimulates intestinal stem cells to differentiate to Paneth cells and enhances luminal secretion of α-defensins. Administration of R-Spo1 or recombinant α-defensin prevents GVHD-mediated dysbiosis, thus representing a novel and physiological approach at modifying the gut ecosystem to restore intestinal homeostasis and host-microbiota cross talk toward therapeutic benefits.

MeSH terms

  • Administration, Oral
  • Animals
  • Bacteria / metabolism
  • Cell Differentiation / drug effects
  • Cytoprotection / drug effects
  • Dysbiosis / etiology*
  • Dysbiosis / pathology
  • Dysbiosis / prevention & control*
  • Female
  • Graft vs Host Disease / complications*
  • Graft vs Host Disease / pathology
  • Humans
  • Intestines / pathology
  • Mice, Inbred C57BL
  • Paneth Cells / drug effects
  • Paneth Cells / metabolism
  • Paneth Cells / pathology*
  • Recombinant Proteins / administration & dosage
  • Recombinant Proteins / pharmacology
  • Recombinant Proteins / therapeutic use
  • Stem Cell Transplantation
  • Stem Cells / drug effects
  • Stem Cells / metabolism
  • Thrombospondins / pharmacology*
  • Thrombospondins / therapeutic use*
  • alpha-Defensins / metabolism

Substances

  • RSPO1 protein, human
  • Recombinant Proteins
  • Thrombospondins
  • alpha-Defensins