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曼氏血吸虫抗原调节卵清蛋白诱导的气道炎症小鼠模型中的过敏反应。

Schistosoma mansoni antigens modulate the allergic response in a murine model of ovalbumin-induced airway inflammation.

机构信息

Serviço de Imunologia, Hospital Universitário Prof Edgard Santos, Universidade Federal da Bahia, Salvador, BA, Brazil.

出版信息

Clin Exp Immunol. 2010 May;160(2):266-74. doi: 10.1111/j.1365-2249.2009.04084.x. Epub 2010 Feb 2.

DOI:10.1111/j.1365-2249.2009.04084.x
PMID:20132231
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2857950/
Abstract

Schistosoma mansoni infection has been associated with protection against allergies. The mechanisms underlying this association may involve regulatory cells and cytokines. We evaluated the immune response induced by the S. mansoni antigens Sm22.6, PIII and Sm29 in a murine model of ovalbumin (OVA)-induced airway inflammation. BALB/c mice were sensitized with subcutaneously injected OVA-alum and challenged with aerolized OVA. Mice were given three doses of the different S. mansoni antigens. Lung histopathology, cellularity of bronchoalveolar lavage (BAL) and eosinophil peroxidase activity in lung were evaluated. Immunoglobulin (Ig)E levels in serum and cytokines in BAL were also measured. Additionally, we evaluated the frequency of CD4+forkhead box P3 (FoxP3)+ T cells in cultures stimulated with OVA and the expression of interleukin (IL)-10 by these cells. The number of total cells and eosinophils in BAL and the levels of OVA-specific IgE were reduced in the immunized mice. Also, the levels of IL-4 and IL-5 in the BAL of mice immunized with PIII and Sm22.6 were decreased, while the levels of IL-10 were higher in mice immunized with Sm22.6 compared to the non-immunized mice. The frequency of CD4+FoxP3+ T cells was higher in the groups of mice who received Sm22.6, Sm29 and PIII, being the expression of IL-10 by these cells only higher in mice immunized with Sm22.6. We concluded that the S. mansoni antigens used in this study are able to down-modulate allergic inflammatory mediators in a murine model of airway inflammation and that the CD4+FoxP3+ T cells, even in the absence of IL-10 expression, might play an important role in this process.

摘要

曼氏血吸虫感染与过敏保护有关。这种关联的机制可能涉及调节细胞和细胞因子。我们在卵清蛋白(OVA)诱导的气道炎症的小鼠模型中评估了 S. mansoni 抗原 Sm22.6、PIII 和 Sm29 诱导的免疫反应。BALB/c 小鼠通过皮下注射 OVA-明矾进行致敏,并通过雾化 OVA 进行挑战。给小鼠三种不同的 S. mansoni 抗原。评估肺组织病理学、支气管肺泡灌洗液(BAL)细胞数和肺中嗜酸性粒细胞过氧化物酶活性。还测量血清中的免疫球蛋白(Ig)E 水平和 BAL 中的细胞因子。此外,我们评估了在 OVA 刺激下培养物中 CD4+叉头框 P3(FoxP3)+T 细胞的频率以及这些细胞中白细胞介素(IL)-10 的表达。免疫小鼠 BAL 中的总细胞和嗜酸性粒细胞数量以及 OVA 特异性 IgE 水平降低。此外,用 PIII 和 Sm22.6 免疫的小鼠 BAL 中的 IL-4 和 IL-5 水平降低,而用 Sm22.6 免疫的小鼠的 IL-10 水平高于未免疫的小鼠。在接受 Sm22.6、Sm29 和 PIII 的小鼠组中,CD4+FoxP3+T 细胞的频率更高,而这些细胞中仅 IL-10 的表达在 Sm22.6 免疫的小鼠中更高。我们得出结论,本研究中使用的 S. mansoni 抗原能够下调气道炎症的小鼠模型中的过敏炎症介质,即使缺乏 IL-10 表达,CD4+FoxP3+T 细胞也可能在该过程中发挥重要作用。

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本文引用的文献

1
Schistosoma mansoni tegument protein Sm29 is able to induce a Th1-type of immune response and protection against parasite infection.曼氏血吸虫表皮蛋白 Sm29 能够诱导 Th1 型免疫应答和对寄生虫感染的保护。
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Schistosoma mansoni antigens modulate experimental allergic asthma in a murine model: a major role for CD4+ CD25+ Foxp3+ T cells independent of interleukin-10.曼氏血吸虫抗原在小鼠模型中调节实验性变应性哮喘:CD4+ CD25+ Foxp3+ T细胞发挥主要作用且不依赖白细胞介素-10
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Schistosoma japonicum infection modulates the development of allergen-induced airway inflammation in mice.日本血吸虫感染可调节小鼠变应原诱导的气道炎症的发展。
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Pulmonary eosinophilia correlates with allergen deposition to the lower respiratory tract in a mouse model of asthma.在哮喘小鼠模型中,肺嗜酸性粒细胞增多与变应原在下呼吸道的沉积相关。
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Helminth-derived products inhibit the development of allergic responses in mice.蠕虫衍生产品可抑制小鼠过敏反应的发展。
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Intestinal helminths protect in a murine model of asthma.肠道蠕虫在哮喘小鼠模型中具有保护作用。
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Human antibody responses of patients living in endemic areas for schistosomiasis to the tegumental protein Sm29 identified through genomic studies.通过基因组研究确定的血吸虫病流行地区患者对皮层蛋白Sm29的人抗体反应。
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Immunization with Schistosoma mansoni 22.6 kDa antigen induces partial protection against experimental infection in a recombinant protein form but not as DNA vaccine.用曼氏血吸虫22.6 kDa抗原进行免疫接种,以重组蛋白形式可诱导对实验性感染的部分保护,但以DNA疫苗形式则不能。
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Helminth-modified pulmonary immune response protects mice from allergen-induced airway hyperresponsiveness.蠕虫改变的肺部免疫反应可保护小鼠免受变应原诱导的气道高反应性影响。
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