B-1 cells modulate the murine macrophage response to Leishmania major infection.
B-1 cells modulate the murine macrophage response to Leishmania major infection.
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DOI：
10.4331/wjbc.v8.i2.151
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发表时间：
2017-05-26
期刊：
影响因子：
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通讯作者：
Freire-de-Lima CG
中科院分区：
文献类型：
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作者：
Arcanjo AF;Nunes MP;Silva-Junior EB;Leandro M;da Rocha JDB;Morrot A;Decote-Ricardo D;Freire-de-Lima CG
探讨B-1细胞对感染硕大利什曼原虫的小鼠腹腔巨噬细胞的调节作用。主要）体外。BALB/c和BALB/c XID小鼠腹腔巨噬细胞感染L.主要，并在存在或不存在从野生型BALB/c小鼠获得的B-1细胞的情况下培养。对细胞内无鞭毛体进行计数，并使用酶联免疫吸附试验定量细胞上清液中的白细胞介素-10（IL-10）产生。使用前列腺素E2酶免疫测定试剂盒（Cayman Chemical，安阿伯，MI）测定脂质介质前列腺素E2（PGE 2）的水平，并在存在和不存在B-1细胞的情况下定量感染的巨噬细胞的细胞质中脂质体的数量。用选择性PGE2中和药物培养细胞抑制PGE2的产生，并证实了这种脂质介质在IL-10产生中的作用。相反，我们证明来源于IL-10 KO小鼠的B-1细胞不利于L.少校我们报道了B-1细胞促进L.腹腔巨噬细胞内的主要无鞭毛体。我们证明了这种调节作用不依赖于细胞之间的物理接触，这表明可溶性因子被释放到培养物中。我们在我们的共培养系统中证明了B-1细胞触发L.严重感染的巨噬细胞IL-10分泌的增加可能与脂质介质PGE 2的存在有关。严重感染的巨噬细胞B-1细胞的存在也有利于受感染的巨噬细胞产生脂质体。相反，我们未能获得相同的效果，寄生虫复制内L。当从IL-10敲除小鼠中分离B-1细胞时，我们的研究结果表明，由B-1细胞产生的PGE 2和IL-10水平的升高使L.主要生长，如细胞培养物中寄生虫的数量所示。
To investigate the modulatory effect of B-1 cells on murine peritoneal macrophages infected with Leishmania major (L. major) in vitro. Peritoneal macrophages obtained from BALB/c and BALB/c XID mice were infected with L. major and cultured in the presence or absence of B-1 cells obtained from wild-type BALB/c mice. Intracellular amastigotes were counted, and interleukin-10 (IL-10) production was quantified in the cellular supernatants using an enzyme-linked immunosorbent assay. The levels of the lipid mediator prostaglandin E2 (PGE2) were determined using a PGE2 enzyme immunoassay kit (Cayman Chemical, Ann Arbor, MI), and the number of lipid bodies was quantified in the cytoplasm of infected macrophages in the presence and absence of B-1 cells. Culturing the cells with selective PGE2-neutralizing drugs inhibited PGE2 production and confirmed the role of this lipid mediator in IL-10 production. In contrast, we demonstrated that B-1 cells derived from IL-10 KO mice did not favor the intracellular growth of L. major. We report that B-1 cells promote the growth of L. major amastigotes inside peritoneal murine macrophages. We demonstrated that the modulatory effect was independent of physical contact between the cells, suggesting that soluble factor(s) were released into the cultures. We demonstrated in our co-culture system that B-1 cells trigger IL-10 production by L. major-infected macrophages. Furthermore, the increased secretion of IL-10 was attributed to the presence of the lipid mediator PGE2 in supernatants of L. major-infected macrophages. The presence of B-1 cells also favors the production of lipid bodies by infected macrophages. In contrast, we failed to obtain the same effect on parasite replication inside L. major-infected macrophages when the B-1 cells were isolated from IL-10 knockout mice. Our results show that elevated levels of PGE2 and IL-10 produced by B-1 cells increase L. major growth, as indicated by the number of parasites in cell cultures.