Arginase I induction during Leishmania major infection mediates the development of disease
Arginase I induction during Leishmania major infection mediates the development of disease
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DOI：
10.1128/iai.73.9.6085-6090.2005
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发表时间：
2005-09-01
影响因子：
3.1
通讯作者：
Corraliza, I
中科院分区：
文献类型：
--
作者：
Iniesta, V;Carcelé, J;Corraliza, I
在之前的工作中，我们证明了精氨酸酶I的诱导有利于利什曼原虫在巨噬细胞内的复制。现在我们已经分析了该酶在主要乳杆菌感染小鼠模型中的差异表达。我们的结果表明，在疾病的发展过程中，精氨酸酶I在易感和耐药小鼠中都被诱导。然而，在感染BALB/c的组织中，该蛋白的诱导与感染时间平行，而在C57BL/6小鼠中，该酶仅在足肿胀期间上调。白介素4(IL-4)和白介素12(IL-12)之间的平衡与一氧化氮合酶11的表达相反，它们对宿主精氨酸酶的诱导是由IL-4和IL-12之间的平衡所介导的。此外，抑制精氨酸酶可减少BALB/c小鼠的寄生虫数量并延迟疾病转归，而L鸟氨酸治疗则增加了C57BL/6小鼠的易感性。因此，精氨酸酶I的诱导可被认为是利什曼病的一个疾病标志物。
In a previous work, we demonstrated that the induction of arginase I favored the replication of Leishmania inside macrophages. Now we have analyzed the differential expression of this enzyme in the mouse model of L. major infection. Ours results show that arginase I is induced in both susceptible and resistant mice during the development of the disease. However, in BALB/c-infected tissues, the induction of this protein parallels the time of infection, while in C57BL/6 mice, the enzyme is upregulated only during footpad swelling. The induction of the host arginase in both strains is mediated by the balance between interleukin-4 (IL-4) and IL-12 and opposite to nitric oxide synthase 11 expression. Moreover, inhibition of arginase reduces the number of parasites and delays disease outcome in BALB/c mice, while treatment with L-ornithine increases the susceptibility of C57BL/6 mice. Therefore, arginase I induction could be considered a marker of disease in leishmaniasis.