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首页> 美国卫生研究院文献>Clinical and Diagnostic Laboratory Immunology >Conjugation of Hydroxyethyl Starch to Desferrioxamine (DFO) Modulates the Dual Role of DFO in Yersinia enterocolitica Infection
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Conjugation of Hydroxyethyl Starch to Desferrioxamine (DFO) Modulates the Dual Role of DFO in Yersinia enterocolitica Infection

机译：羟乙基淀粉与去铁胺（DFO）的结合调节DFO在小肠结肠炎耶尔森氏菌感染中的双重作用

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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.
机译：铁螯合剂去铁胺（DFO）B被广泛用于铁超负荷患者的治疗。作为副作用，DFO可能有助于发生暴发性耶尔森氏菌感染。我们实验室的先前工作表明，这可能是由于DFO的双重作用：促进病原体的生长和宿主的免疫抑制。在这项研究中，我们试图确定DFO与羟乙基淀粉（HES-DFO）的结合是否可以预防小鼠耶尔森氏菌感染的恶化。我们发现HES-DFO既不促进小肠结肠炎耶尔森氏菌的生长，又不促进有丝分裂原诱导的T细胞增殖和体外T细胞产生的γ干扰素。然而，体内的HES-DFO可能由于HES的裂解和DFO的释放而促进了小肠结肠炎耶尔森氏菌的生长。用DFO预处理的小鼠在应用正常致死性小肠结肠炎耶尔森菌接种后2至5天导致所有小鼠死亡，而用HES-DFO预处理的小鼠均未在感染后的前7天死亡。但是，某些HES-DFO处理的小鼠在感染后8到14天死亡。因此，由于延迟的体内作用，HES-DFO无法触发耶尔森氏菌引起的败血性休克，这解释了DFO相关败血病的早期死亡率。此外，我们的数据表明，DFO需要被宿主细胞吸收才能发挥其免疫抑制作用。这些结果强烈表明，就DFO促进的暴发性感染而言，HES-DFO可能是一种比DFO副作用少的有益药物。

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