实验性兔蛔虫病易感和耐药小鼠脾脏细胞的分析。

ISRN Parasitology Pub Date : 2012-09-12 eCollection Date: 2013-01-01 DOI:10.5402/2013/180652
Priscila Guirão Lara, Mariana Felix de Souza Prudente, Neusa Mariana Costa Dias, Denise Vilarinho Tambourgi, Ruy de Souza Lino-Junior, Mônica Spadafora-Ferreira, Mara Silvia Carvalhaes
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摘要

Lagochilascaris是由小Lagochilascaris引起的一种新出现的寄生虫病。用实验小鼠模型研究了对小乳杆菌感染的免疫反应。在本工作中,免疫组织化学分析了实验感染小乳杆菌的易感(C57BL/6)和耐药(BALB/c)小鼠的脾脏细胞群。BALB/c小鼠在感染后100天脾脏细胞指数(DPI)为F4/80+, 100和250 DPI为CD4+, 35和100 DPI为CD8+, 100、150和250 DPI为CD19+。在感染C57BL/6小鼠的脾脏中,观察到以下脾脏细胞指数的增加:250 DPI时F4/80+细胞,150 DPI时CD4+细胞,35、150、250 DPI时CD8+细胞,150 ~ 250 DPI时CD19+细胞。脾细胞指数证实了对照组和感染组在感染后几个时间点的差异。这些数据表明,在BALB/c小鼠中,CD4+和CD19+脾脏细胞数量的优先增加与实验性lagochil蛔虫病的抗性之间存在关联,在C57BL/6小鼠中,CD8+脾脏细胞数量的优先增加与易感性之间存在关联。
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Analysis of Spleen Cells in Susceptible and Resistant Mice with Experimental Lagochilascariosis.

Lagochilascariosis is an emerging parasitic disease caused by the helminth Lagochilascaris minor. The experimental mouse model has been used to study the immune response against L. minor infection. In the present work, immunohistochemistry analysis of spleen cells populations was evaluated in susceptible (C57BL/6) and resistant (BALB/c) mice experimentally infected with L. minor. The BALB/c mice exhibited increased spleen cell indexes as follows: F4/80+ at 100 days after infection (DPI), CD4+ at 100 and 250 DPI, CD8+ at 35 and 100 DPI, and CD19+ at 100, 150, and 250 DPI. In the spleens of the infected C57BL/6 mice, increased indexes of the following spleen cells were observed: F4/80+ cells at 250 DPI, CD4+ cells at 150 DPI, CD8+ cells at 35, 150, and 250 DPI, and CD19+ cells at 150 to 250 DPI. The index of spleen cells confirmed the differences between the control and infected groups at several time points following the infection. These data demonstrate an association between a preferential increase in the number of CD4+ and CD19+ spleen cells and resistance to experimental lagochilascariosis in BALB/c mice and between a preferential increase in the number of CD8+ spleen cells and susceptibility in C57BL/6 mice.

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