Eosinophils suppress Th1 responses and restrict bacterially induced gastrointestinal inflammation

J Exp Med. 2018 Aug 6;215(8):2055-2072. doi: 10.1084/jem.20172049. Epub 2018 Jul 3.


Eosinophils are predominantly known for their contribution to allergy. Here, we have examined the function and regulation of gastrointestinal eosinophils in the steady-state and during infection with Helicobacter pylori or Citrobacter rodentium We find that eosinophils are recruited to sites of infection, directly encounter live bacteria, and activate a signature transcriptional program; this applies also to human gastrointestinal eosinophils in humanized mice. The genetic or anti-IL-5-mediated depletion of eosinophils results in improved control of the infection, increased inflammation, and more pronounced Th1 responses. Eosinophils control Th1 responses via the IFN-γ-dependent up-regulation of PD-L1. Furthermore, we find that the conditional loss of IFN-γR in eosinophils phenocopies the effects of eosinophil depletion. Eosinophils further possess bactericidal properties that require their degranulation and the deployment of extracellular traps. Our results highlight two novel functions of this elusive cell type and link it to gastrointestinal homeostasis and anti-bacterial defense.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Disease
  • Animals
  • Antibodies, Bacterial / immunology
  • Bacterial Infections / immunology
  • Bacterial Infections / microbiology
  • Bacterial Infections / pathology
  • Cell Degranulation
  • Cell Proliferation
  • Citrobacter rodentium / physiology*
  • Colitis / immunology
  • Colitis / microbiology
  • Colitis / pathology
  • Cytokines / biosynthesis
  • Disease Models, Animal
  • Eosinophils / immunology*
  • Eosinophils / physiology
  • Extracellular Traps / metabolism
  • Gastrointestinal Tract / immunology
  • Gastrointestinal Tract / microbiology*
  • Gastrointestinal Tract / pathology*
  • Helicobacter pylori / physiology*
  • Homeostasis
  • Immunity, Innate
  • Immunity, Mucosal
  • Inflammation / immunology*
  • Inflammation / microbiology*
  • Inflammation / pathology
  • Interferon-gamma / metabolism
  • Mice, Inbred C57BL
  • Signal Transduction
  • Th1 Cells / immunology*
  • Th17 Cells / immunology


  • Antibodies, Bacterial
  • Cytokines
  • Interferon-gamma