Comparison of Iron-Reduced and Iron-Supplemented Semisynthetic Diets in T Cell Transfer Colitis

PLoS One. 2019 Jul 5;14(7):e0218332. doi: 10.1371/journal.pone.0218332. eCollection 2019.


Clinical observations in inflammatory bowel disease patients and experimental studies in rodents suggest that iron in the intestinal lumen derived from iron-rich food or oral iron supplementation could exacerbate inflammation and that iron depletion from the diet could be protective. To test the hypothesis that dietary iron reduction is protective against colitis development, the impact of iron reduction in the diet below 10 mg/kg on the course of CD4+ CD62L+ T cell transfer colitis was investigated in adult C57BL/6 mice. Weight loss as well as clinical and histological signs of inflammation were comparable between mice pretreated with semisynthetic diets with either < 10mg/kg iron content or supplemented with 180 mg/kg iron in the form of ferrous sulfate or hemin. Accumulation and activation of Ly6Chigh monocytes, changes in dendritic cell subset composition and induction of proinflammatory Th1/Th17 cells in the inflamed colon were not affected by the iron content of the diets. Thus, dietary iron reduction did not protect adult mice against severe intestinal inflammation in T cell transfer induced colitis.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adoptive Transfer
  • Animals
  • Colon / immunology
  • Colon / pathology
  • Dendritic Cells / immunology
  • Dendritic Cells / pathology
  • Dietary Supplements*
  • Disease Models, Animal
  • Food, Formulated*
  • Inflammatory Bowel Diseases* / diet therapy
  • Inflammatory Bowel Diseases* / immunology
  • Inflammatory Bowel Diseases* / pathology
  • Iron / pharmacology*
  • Mice
  • Mice, Knockout
  • Monocytes / immunology
  • Monocytes / pathology
  • Th1 Cells* / immunology
  • Th1 Cells* / pathology
  • Th1 Cells* / transplantation
  • Th17 Cells* / immunology
  • Th17 Cells* / pathology
  • Th17 Cells* / transplantation


  • Iron

Grant support

A.M. A.H., A.K. W.R. and D.H. were supported by the GRK 1482 of the German Research Foundation. A.K., A.H. E.D, R.M., L.J. and K.E. received funding from German Research Foundation grants SFB1054/TPA06, KR2199/3-2, KR2199/6-1, KR2199/9-1. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.