Enhanced expression of colonic non-heme iron transporters divalent metal transporter-1 (DMT-1) and ferroportin (FPN) in patients with ulcerative colitis

Iron is an essential micronutrient that is involved in many different physiological processes, such as redox reactions of the electron transport chain, oxygen transport, and DNA synthesis. Additionally, iron is an important limiting factor for microbial growth. The tight regulation of whole body and cellular iron concentration is part of the innate immune system whereby the body can restrict the amount of available iron to help prevent the growth of pathogenic bacteria. This is crucial because microbial dysbiosis is detrimental to health and is thought to play a causative role in the development of ulcerative colitis (UC), a chronic inflammatory bowel disease (IBD) associated with bloody, mucous‐laden stools. Patients with ulcerative colitis (UC) frequently suffer from iron deficiency and may be prescribed oral iron supplementation, but there is fine line between trying to correct the iron deficiency and providing excess iron that can exacerbate disease activity and alter the microbial community. Most iron absorption occurs in the duodenum, but the colon is also known to contain non‐heme iron transporters. The purpose of this study was to characterize the location of iron transporters in normal human colon and determine whether their expression varied in patients with UC. RNA and protein were isolated from colonic biopsy specimens obtained during previously scheduled colonoscopies. We found a trend of decreasing mRNA and protein abundance from the cecum to the distal colon of DMT‐1 and FPN. Patients with ulcerative colitis had increased expression of colonic iron transporters, with the highest expression of those transporters found in patients with active disease activity. The upregulation of iron transporters in the colonic epithelium of patients with UC may have a two‐fold benefit: increased colonic iron absorption would help alleviate the iron deficiency frequently seen in patients with UC and it would limit the amount of available iron in the colonic lumen, thus reducing the growth of pathogenic bacteria. Support or Funding Information R01: 10019896.1.1006856R This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .