Heme oxygenase-1 confers protection and alters T-cell populations in a mouse model of neonatal intestinal inflammation

Pediatr Res. 2015 May;77(5):640-8. doi: 10.1038/pr.2015.22. Epub 2015 Feb 9.

Abstract

Background: Necrotizing enterocolitis (NEC), an intestinal inflammatory disease affecting premature infants, is associated with low regulatory T (Treg) to effector T (Teff) cell ratios. We recently demonstrated that heme oxygenase-1 (HO-1) deficiency leads to increased NEC development. Here, we investigated the effects of HO-1 on T-cell proportions in a murine NEC-like injury model.

Methods: Intestinal injury was induced in 7-d-old wild-type (WT) or HO-1 heterozygous (HO-1 Het) pups by formula-feeding every 4 h for 24-78 h by oral gavage and exposures to 5%O2. Controls remained breastfed. HO-1 was induced in WT pups by administering heme preinjury induction. Lamina propria T cells were identified by flow cytometry. For adoptive transfer studies, WT splenic/thymic Tregs were injected intraperitoneally into HO-1 Het pups 12-24 h preinduction.

Results: Het mice showed increased intestinal injury and decreased Treg/Teff ratios. Genes for pattern recognition (Toll-like receptor-4, C-reactive protein, MyD88) and neutrophil recruitment increased in Het pups after NEC induction. Inducing intestinal HO-1 decreased NEC scores and incidence, and increased Treg/Teff ratios. Moreover, adoptive transfer of Tregs from WT to HO-1 Het pups decreased NEC scores and incidence and restored Treg/Teff ratios.

Conclusion: HO-1 can change Treg proportions in the lamina propria of young mice under inflammatory conditions, which might, in part, confer intestinal protection.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptive Immunity
  • Adoptive Transfer
  • Animals
  • CD4-Positive T-Lymphocytes / cytology
  • CD8-Positive T-Lymphocytes / cytology
  • Disease Models, Animal
  • Female
  • Flow Cytometry
  • Genotype
  • Heme Oxygenase-1 / genetics*
  • Heme Oxygenase-1 / physiology*
  • Heterozygote
  • Humans
  • Infant, Newborn
  • Inflammation / pathology*
  • Interleukin-2 Receptor alpha Subunit / metabolism
  • Intestines / pathology*
  • Male
  • Membrane Proteins / genetics*
  • Membrane Proteins / physiology*
  • Mice
  • Mucous Membrane / metabolism
  • Phenotype
  • T-Lymphocytes, Regulatory / cytology*
  • Time Factors

Substances

  • Interleukin-2 Receptor alpha Subunit
  • Membrane Proteins
  • Heme Oxygenase-1
  • Hmox1 protein, mouse