AI Article Synopsis

  • The study investigated how acute and chronic inflammation affects proteins related to iron absorption in mice, specifically looking at changes in duodenal proteins, liver hepcidin, and serum iron levels.
  • Following acute inflammation from turpentine, mice showed increased ferritin levels early on, followed by decreased expression of a transporter for iron and later changes in hepatic hepcidin and ferroportin, leading to initial low iron levels.
  • When inflammation resolved, many of these changes were reduced; however, chronic inflammation showed more variable effects, indicating complex interactions between inflammation and iron regulation.

Article Abstract

In order to understand better the molecular mechanisms involved in the pathogenesis of anaemia of inflammation, we carried out a time-course study on the effects of turpentine-induced acute and chronic inflammation on duodenal proteins involved in Fe absorption in mice. Expression levels of these proteins and hepatic hepcidin and serum Fe levels were determined in inflamed mice. In acutely inflamed mice, significantly increased expression of ferritin was the earliest change observed, followed by decreased divalent metal transporter 1 expression in the duodenum and increased hepcidin expression in the liver. Ferroportin expression increased subsequently, despite high levels of hepcidin. Hypoferraemia, which developed at early time periods studied, was followed by increased serum Fe levels at later points. The present results thus show that acute inflammation induced several changes in the expression of proteins involved in duodenal Fe absorption, contributing to the development of hypoferraemia. Resolution of inflammation caused attenuation of many of these effects. Effects in chronically inflamed mice were less consistent. The present results also suggest that inflammation-induced increases in ferritin appeared to override the effects of hepcidin on the expression levels of ferroportin in enterocytes.

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http://dx.doi.org/10.1017/S0007114512000189DOI Listing

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