Entamoeba histolytica cysteine protease 2 (EhCP2) modulates leucocyte migration by proteolytic cleavage of chemokines
Entamoeba histolytica cysteine protease 2 (EhCP2) modulates leucocyte migration by proteolytic cleavage of chemokines
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DOI：
10.1111/j.0141-9838.2004.00706.x
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发表时间：
2004-05-01
影响因子：
2.2
通讯作者：
García-Zepeda, E
中科院分区：
文献类型：
--
作者：
Belloso, SP;Saloma, PO;García-Zepeda, E
人类阿米巴病是一种由原生动物溶组织内阿米巴感染引起的疾病，目前影响着全世界数百万人。阿米巴结肠炎是最常见的临床表现。宿主保护性免疫涉及体液和细胞反应的参与。然而，免疫逃避的机制尚不清楚，仍在研究中。这些机制之一可能与寄生虫蛋白酶调节或干扰炎症过程的能力有关，炎症过程是由促炎细胞因子（例如趋化因子）的表达引发的。为了进一步阐明半胱氨酸蛋白酶在调节趋化因子介导功能中的潜在作用，我们分析了溶组织内阿米巴半胱氨酸蛋白酶 2 (EhCP2) 通过趋化因子裂解对白细胞趋化性产生影响的能力。我们发现EhCP2能够裂解趋化因子CCL2、CCL13和CXCL8，并且与完整趋化因子诱导的趋化性相比，所产生的蛋白水解产物调节白细胞的趋化性。因此，半胱氨酸蛋白酶的细胞外活性影响趋化因子介导的反应，并且可以被认为是溶组织内阿米巴用来规避宿主免疫反应的机制的一部分。
Human amoebiasis is a disease produced by infection with the protozoan Entamoeba histolytica currently affecting many millions of people worldwide. Amoebic colitis is the most common clinical manifestation. Host protective immunity involves participation of both humoral and cellular responses. However, the mechanisms involved in immune evasion are not clear and remain under investigation. One of these mechanisms could be associated with the ability of parasite proteases to modulate or interfere with the inflammation process, which is initiated by expression of pro-inflammatory cytokines such as chemokines. To further clarify the potential role of cysteine proteases in modulating chemokine-mediated functions, we have analysed the ability of Entamoeba histolytica cysteine protease 2 (EhCP2) to have an effect on the chemotaxis of leucocytes by chemokine cleavage. We find that EhCP2 is capable of cleaving chemokines CCL2, CCL13 and CXCL8, and the resulting proteolysis products modulate the chemotaxis of leucocytes when compared to that induced by intact chemokine. Thus, the extracellular activity of the cysteine proteases affects chemokine-mediated responses and could be considered as part of the mechanisms used by Entamoeba histolytica to circumvent the host immune responses.