Low iron availability modulates the course of Chlamydia pneumoniae infection

Chlamydiae are obligate intracellular bacteria residing exclusively in host cell vesicles termed inclusions. We have investigated the effects of defer oxamine mesylate (DAM)-induced iron deficiency on the growth of Chlamydia p neumoniae and Chlamydia trachomatis serovar L2. In epithelial cells subject ed to iron starvation and infected with either C. pneumoniae or C. trachoma tis L2, small inclusions were formed, and the infectivity of chlamydial pro geny was impaired. Moreover, for C. trachomatis L2, we observed a delay in homotypic fusion of inclusions. The inhibitory effects of DAM were reversed by adding exogenous iron-saturated transferrin, which restored the product ion of infectious chlamydiae. Electron microscopy examination of iron-depri ved specimens revealed that the small inclusions contained reduced numbers of C. pneumoniae that were mostly reticulate bodies. We have previously rep orted specific accumulation of transferrin receptors (TfRs) around C. pneum oniae inclusions within cells grown under normal conditions. Using confocal and electron microscopy, we show here a remarkable increase in the amount of TfRs surrounding the inclusions in iron-starved cultures. It has been sh own that iron is an essential factor in the growth and survival of C. trach omatis. Here, we postulate that, for C. pneumoniae also, iron is an indispe nsable element and that Chlamydia may use iron transport pathways of the ho st by attracting TfR to the phagosome.