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首页> 外文期刊>Infection and immunity >Interleukin-6-Driven Inflammatory Response Induces Retinal Pathology in a Model of Ocular Toxoplasmosis Reactivation
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Interleukin-6-Driven Inflammatory Response Induces Retinal Pathology in a Model of Ocular Toxoplasmosis Reactivation

机译：白细胞介素6驱动的炎症反应诱导眼弓形虫病再激活模型中的视网膜病理。

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Ocular inflammation is one of the consequences of infection with the protozoan parasite Toxoplasma gondii. Even if lesions are self-healing in immunocompetent persons, they pose a lifetime risk of reactivation and are a serious threat to vision. As there are virtually no immunological data on reactivating ocular toxoplasmosis, we established a model of direct intravitreal injection of parasites in previously infected mice with a homologous type II strain. Two different mouse strains with variable ability to control retinal infection were studied in order to describe protective and deleterious reaction patterns. In Swiss-Webster mice, which are already relatively resistant to primary infection, no peak of parasite load was observed upon reinfection. In contrast, the susceptible inbred strain C57BL/6 showed high parasite loads after 7 days, as well as marked deterioration of retinal architecture. Both parameters were back to normal on day 21. C57BL/6 mice also reacted with a strong local production of inflammatory and Th1-type cytokines, like interleukin-6 (IL-6), IL-17A, and gamma interferon (IFN-γ), while Swiss-Webster mice showed only moderate expression of the Th2 cytokine IL-31. Interestingly, rapid intraocular production of anti-Toxoplasma antibodies was observed in Swiss-Webster but not in C57BL/6 mice. We then localized the cellular source of different immune mediators within the retina by immunofluorescence. Finally, neutralization experiments of IFN-γ or IL-6 demonstrated the respective protective and deleterious roles of these cytokines for parasite control and retinal integrity during reinfection. In conclusion, we developed and immunologically characterized a promising mouse model of reactivating ocular toxoplasmosis.
机译：眼部炎症是原生动物寄生虫弓形虫感染的后果之一。即使病变在具有免疫能力的人中能够自愈，它们也可能终生重新激活，并且严重威胁视力。由于实际上没有关于重新激活眼弓形虫病的免疫学数据，我们建立了在先前感染过同源II型毒株的小鼠体内直接玻璃体内注射寄生虫的模型。为了描述保护性和有害反应模式，研究了两种具有可变能力来控制视网膜感染的不同小鼠品系。在已经对原发感染具有相对抗性的Swiss-Webster小鼠中，再感染后未观察到寄生虫负荷的峰值。相反，易感近交菌株C57BL / 6在7天后显示出较高的寄生虫负荷，并且视网膜结构显着恶化。这两个参数均在第21天恢复正常。C57BL/ 6小鼠还与炎症和Th1型细胞因子（如白介素6（IL-6），IL-17A和γ干扰素（IFN-γ））的强烈局部产生反应），而Swiss-Webster小鼠仅显示Th2细胞因子IL-31的中等表达。有趣的是，在Swiss-Webster中观察到了抗弓形虫抗体的快速眼内生成，但在C57BL / 6小鼠中却没有。然后，我们通过免疫荧光定位了视网膜内不同免疫介质的细胞来源。最后，IFN-γ或IL-6的中和实验证明了这些细胞因子在再感染过程中对寄生虫控制和视网膜完整性的各自保护和有害作用。总之，我们开发了一种有希望的激活眼弓形虫病的小鼠模型并对其进行了免疫学表征。

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