Macrophage migration inhibitory factor homolog from Plasmodium yoelii modulates monocyte recruitment and activation in spleen during infection
文献类型： 外文期刊
作者： Zhang, Yanhui 1 ; Miura, Kazutoyo 1 ; Li, Jian 1 ; Tullo, Gregory 1 ; Zhu, Feng 2 ; Hong, Lingxian 2 ; Lin, Tianlong 3 ;
作者机构： 1.NIAID, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA
2.Xiamen Univ, State Key Lab Stress Cell Biol, Sch Life Sci, Xiamen 361005, Fujian, Peoples R China
3.Fujian Acad Agr Sci, Fuzhou 350002, Fujian, Peoples R China
期刊名称：PARASITOLOGY RESEARCH （ 影响因子：2.289； 五年影响因子：2.403 ）
ISSN： 0932-0113
年卷期： 2012 年 110 卷 5 期
页码：
收录情况： SCI
摘要： Macrophage migration inhibitory factor (MIF) has been shown to be involved in the pathogenesis of severe malaria. Malaria parasites express an MIF homolog that may play a role in regulating host immune responses, and a recent study showed that overexpression of MIF reduced parasitemia in a mouse malaria model. Another recent study showed migration of monocytes to the spleen contributed to the control of blood stage infection. However, there are few papers describing the effect of MIF on monocyte recruitment/activation during the infection. We generated recombinant Plasmodium yoelii MIF (rPyMIF) and investigated its function on purified mouse CD11b(+) cells in vitro and monocyte responses in vivo. The result shows that rPyMIF protein bound to mouse CD11b(+) cells and inhibited their random migration in vitro. On the other hand, rPyMIF did not induce cytokine release from the cells directly or modulate lipopolysaccharide-induced cytokine release. Mice immunized with rPyMIF showed transient but significantly lower parasitemia than the control mice at day 3 after lethal Py17XL challenge. The total number of CD11b(+) cells in the spleens was significantly higher in rPyMIF-immunized group. Further investigation revealed that there were significantly higher numbers of recruited and activated monocytes in the spleens of rPyMIF immunization group on day 3. These results indicate that PyMIF potentially modulates monocyte recruitment and activation during infection of P. yoelii erythrocytic stages.
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