CD44 mediated hyaluronan adhesion of Toxoplasma gondii-infected leukocytes.

CD44 mediated hyaluronan adhesion of Toxoplasma gondii-infected leukocytes.
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DOI:
10.1016/j.parint.2013.10.008
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发表时间:
2014-04
影响因子:
1.9
通讯作者:
Takeshi Hayashi;A. Unno;Minami Baba;T. Ohno;K. Kitoh;Y. Takashima
Takeshi Hayashi;A. Unno;Minami Baba;T. Ohno;K. Kitoh;Y. Takashima
中科院分区:
医学3区
文献类型:
--
作者:
Takeshi Hayashi;A. Unno;Minami Baba;T. Ohno;K. Kitoh;Y. Takashima

文献摘要

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刚地弓形虫是一种专性细胞内顶复合体寄生虫,感染人类和动物。被摄入的寄生虫穿过肠上皮,侵入白细胞,然后播散到周围器官。然而,感染的白细胞外渗的机制仍然知之甚少。在本研究中,我们证明了t。gondii入侵的人和小鼠白细胞表达更高水平的CD44, CD44是透明质酸(HA)的配体,其在髓细胞和非髓细胞上的表达引起est。刚地虫侵入人类和小鼠白细胞比非侵入白细胞更有效地粘附于透明质酸。抗CD44抗体可抑制寄生虫入侵白细胞的特异性粘附。CD44敲除小鼠的白细胞未表现出寄生虫入侵的白细胞特异性粘附。我们的研究结果表明,寄生虫入侵的白细胞,无论是否髓系,通过上调CD44表达和/或选择性入侵CD44高表达的细胞,比未入侵的白细胞获得更高的粘附HA的能力。被寄生虫入侵的细胞与未被入侵的邻近细胞粘附HA的能力不同,可能有助于将被寄生虫入侵的白细胞有效地运送到产生HA的内皮细胞表面和/或富含HA的细胞外基质。
Toxoplasma gondiiis an obligate intracellular apicomplexan parasite that infects humans and animals. Ingested parasites cross the intestinal epithelium, invade leukocytes and are then disseminated to peripheral organs. However, the mechanism of extravasation of the infected leukocytes remains poorly understood. In this study, we demonstrate thatT. gondii-invaded human and mouse leukocytes express higher level of CD44, a ligand of hyaluronan (HA), and its expression on myeloid and non-myeloid leukocytes causesT. gondii-invaded human and mouse leukocyte to adhere to HA more effectively than non-invaded leukocytes. The specific adherence of parasite-invaded leukocytes was inhibited by anti CD44 antibody. Leukocytes of CD44 knockout mice did not show parasite-invaded leukocyte specific adhesion. Our results indicate that parasite-invaded leukocytes, regardless of whether myeloid or not, gain higher ability to adhere to HA than non-invaded leukocytes, via upregulation of CD44 expression and/or selective invasion to CD44 highly expressing cells. The difference in ability to adhere to HA between parasite-invaded cells and non-invaded neighboring cells might facilitate effective delivery of parasite-invaded leukocytes to the HA-producing endothelial cell surface and/or HA-rich extra cellular matrix.