Differential ferritin expression is associated with iron deficiency in coeliac disease

Sixty percent of people with coeliac disease (CD) are iron deficient. Many, however, remain iron replete despite the disease.

(i) To characterize the changes in duodenal iron transport proteins in CD with and without iron deficiency. (ii) To examine if iron-activated gut lymphocytes can inhibit iron export in an enterocyte cell model.

Endoscopic duodenal biopsies were collected from patients with normal duodenum with and without iron deficiency anaemia and untreated CD sufferers with iron deficiency (n=10 each group). mRNA expression of iron transport proteins was determined by quantitative real time PCR. Protein localization and expression was determined from histology sections in patients with normal duodenum (n=20), and patients with untreated CD with and without iron deficiency (n=20). In addition, CaCo2 cells were cocultured with iron-activated lymphocytes 55Fe was used to determine the effect on CaCo2 cell iron transport.

The expression of divalent metal transporter 1 and ferroportin was increased in CD with or without iron deficiency. Ferritin expression was increased in CD but only in those with associated iron deficiency. TNF-alpha produced by activated lymphocytes inhibited iron export from CaCo2 cells.

Increased enterocyte ferritin expression may promote iron deficiency in CD and this effect seems to be dependent upon TNF-alpha expression in gut lymphocytes.