Abstract

A total number of 13 iron metabolism relation genes expression profiles of RAW264.7 murine macrophages infected or uninfected with Salmonella typhimurium were tested by real-time polymerase chain reaction (RT-PCR) to evaluate the metabolism of iron in host-pathogen interplay. The living wild-type S. typhimurium induces expression of the transferrin receptor (Tfr1) in host cell macrophages, which results in a sustained increase of the labile iron pool inside the host cell after 1  or 24 h infection. Gene expression analysis showed that wild-type S. typhimurium drives an active iron acquisition program with induction of ferrireductase (Steap3), iron membrane transporter Dmt1, and iron regulatory proteins (Irp1 and Irp2), while not too much iron efflux changing through ferriportin (Fpn1). The spiA^- Salmonella mutant strain used in our studies also caused an increase in Tfr1 at 1 or 24 h, but leading to decrease in Fpn1 at 24 h as compared with 1 h. The assessment of the labile iron pool after infection with spiA^- Salmonella after 24 h shows an increase. The same of these two phenotypes allowed iron overload in macrophage and became one of the reasons for Salmonella survival inside the macrophage.

Key words: Macrophage, Salmonella, iron metabolism.