Comparison of iron-reduced and iron-supplemented semisynthetic diets in T cell transfer colitis

Abstract

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 Ly6C high 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.

Regulation of Th1 T Cell Differentiation by Iron via Upregulation of T Cell Immunoglobulin and Mucin Containing Protein-3 (TIM-3)

“…Mice were fed with low (<9 mg elementary Fe/kg) ( 26 ) or high iron (5 g/kg) diets for two weeks and during the course of the infection. After intraperitoneal infection with 500 CFU of S .…”

“…For the infection model male mice were fed with different iron diets for two weeks and during the course of the infection. Low iron diet had an iron content of ≤9 mg iron/kg diet (26), high ion diet contained 5 g iron/kg diet (both diets from Altromin). Male mice were used at 8-12 weeks of age and infected intraperitoneally with 500 CFU of S. Typhimurium in 200 ml PBS (27)(28)(29).…”

Prevention of Adult Colitis by Oral Ferric Iron in Juvenile Mice Is Associated with the Inhibition of the Tbet Promoter Hypomethylation and Gene Overexpression

“…Other hypotheses regarding the effects of chronic iron ingestion may be issued. Indeed, it was reported that iron is involved in the growth and function of immune cells and could modulate the Th1/Th2 ratio by a ROS-mediated mechanism [48,49,50], but contradictory results were found in different studies, possibly due to the form of iron [50,51].…”

Targeting the Microenvironment of Vulnerable Atherosclerotic Plaques: An Emerging Diagnosis and Therapy Strategy for Atherosclerosis

“…[ 125 ] In addition, as second messengers in cell signaling, excess ROS activate the NF‐κB signaling pathway and promote inflammatory cytokine generation. [ 126 ] Therefore, based on the intrinsic ROS‐scavenging properties of nanomaterials, antioxidant therapy is a reasonable and potential strategy for alleviating the development of atherosclerosis.…”