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首页> 外文期刊>Infection and immunity >Granulocyte-Macrophage Colony-Stimulating Factor-Deficient Mice Have Impaired Resistance to Blood-Stage Malaria
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Granulocyte-Macrophage Colony-Stimulating Factor-Deficient Mice Have Impaired Resistance to Blood-Stage Malaria

机译：粒细胞-巨噬细胞集落刺激因子缺乏小鼠对血期疟疾的抵抗力受损

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The contribution of granulocyte-macrophage colony-stimulating factor (GM-CSF), a hematopoietic and immunoregulatory cytokine, to resistance to blood-stage malaria was investigated by infecting GM-CSF-deficient (knockout [KO]) mice with Plasmodium chabaudi AS. KO mice were more susceptible to infection than wild-type (WT) mice, as evidenced by higher peak parasitemia, recurrent recrudescent parasitemia, and high mortality. P. chabaudiAS-infected KO mice had impaired splenomegaly and lower leukocytosis but equivalent levels of anemia compared to infected WT mice. Both bone marrow and splenic erythropoiesis were normal in infected KO mice. However, granulocyte-macrophage colony formation was significantly decreased in these tissues of uninfected and infected KO mice, and the numbers of macrophages in the spleen and peritoneal cavity were significantly lower than in infected WT mice. Serum levels of gamma interferon (IFN-γ) were found to be significantly higher in uninfected KO mice, and the level of this cytokine was not increased during infection. In contrast, IFN-γ levels were significantly above normal levels in infected WT mice. During infection, tumor necrosis factor alpha (TNF-α) levels were significantly increased in KO mice and were significantly higher than TNF-α levels in infected WT mice. Our results indicate that GM-CSF contributes to resistance to P. chabaudi AS infection and that it is involved in the development of splenomegaly, leukocytosis, and granulocyte-macrophage hematopoiesis. GM-CSF may also regulate IFN-γ and TNF-α production and activity in response to infection. The abnormal responses seen in infected KO mice may be due to the lack of GM-CSF during development, to the lack of GM-CSF in the infected mature mice, or to both.
机译：通过用疟原虫感染GM-CSF缺陷型小鼠（敲除[KO]），研究了造血和免疫调节细胞因子粒细胞-巨噬细胞集落刺激因子（GM-CSF）对血液疟疾抵抗力的贡献。 chabaudi AS。 KO小鼠比野生型（WT）小鼠更容易受到感染，这表现为更高的峰值寄生率，复发性复发寄生率和高死亡率。 P。 Chabaudi AS感染的KO小鼠脾脏肿大和白细胞减少，但与感染的WT小鼠相比，贫血水平相当。感染的KO小鼠的骨髓和脾红细胞生成均正常。然而，未感染和感染的KO小鼠的这些组织中的粒细胞-巨噬细胞集落形成显着减少，并且脾脏和腹膜腔中的巨噬细胞数量明显低于感染的WT小鼠。发现未感染的KO小鼠的血清γ干扰素（IFN-γ）的水平明显更高，并且这种细胞因子的水平在感染期间并未增加。相反，在感染的WT小鼠中，IFN-γ水平显着高于正常水平。在感染过程中，KO小鼠中的肿瘤坏死因子α（TNF-α）水平显着升高，并且显着高于感染的WT小鼠中的TNF-α水平。我们的结果表明，GM-CSF有助于抗 P。 chabaudi AS感染，它参与了脾肿大，白细胞增多和粒细胞巨噬细胞造血的发展。 GM-CSF还可能调节IFN-γ和TNF-α的产生以及响应感染的活性。在感染的KO小鼠中看到的异常反应可能是由于发育过程中缺少GM-CSF，感染的成熟小鼠中缺少GM-CSF或两者都有。

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