ArticleClinical and diagnostic laboratory immunology2000
Conjugation of hydroxyethyl starch to desferrioxamine (DFO) modulates the dual role of DFO in Yersinia enterocolitica infection.
Article in Clinical and diagnostic laboratory immunology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 12 citations in OpenAlex.
- Dioxazolium desferrioxamine as a cell permeant chelator of intracellular labile iron.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Article
- Genetic Engineering ofJournal of fungi (Basel, Switzerland) · 2022Article
- Bacterial Siderophores Hijack Neutrophil Functions.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Iron chelators modulate the fusogenic properties of Salmonella-containing phagosomes.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
The iron chelator desferrioxamine (DFO) B is widely used in the therapy of patients with iron overload. As a side effect, DFO may favor the occurrence of fulminant Yersinia infections. Previous work from our laboratory showed that this might be due to a dual role of DFO: growth promotion of the pathogen and immunosuppression of the host. In this study, we sought to determine whether conjugation of DFO to hydroxyethyl starch (HES-DFO) may prevent exacerbation of Yersinia infection in mice. We found HES-DFO to promote neither growth of Yersinia enterocolitica nor mitogen-induced T-cell proliferation and gamma interferon production by T cells in vitro. Nevertheless, in vivo HES-DFO promoted growth of Y. enterocolitica possibly due to cleavage of HES and release of DFO. The pretreatment of mice with DFO resulted in death of all mice 2 to 5 days after application of a normally sublethal inoculum of Y. enterocolitica, while none of the mice pretreated with HES-DFO died within the first 7 days postinfection. However, some of the HES-DFO-treated mice died 8 to 14 days postinfection. Thus, due to the delayed in vivo effect HES-DFO failed to trigger Yersinia-induced septic shock, which accounts for early mortality in DFO-associated septicemia. Moreover, our data suggest that DFO needs to be taken up by host cells in order to exert its immunosuppressive action. These results strongly suggest that HES-DFO might be a favorable drug with fewer side effects than DFO in terms of DFO-promoted fulminant infections.
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