Shibayama Mineko, Rivera-Aguilar Víctor, Barbosa-Cabrera Elizabeth, Rojas-Hernández Saúl, Jarillo-Luna Adriana, Tsutsumi Víctor, Pacheco-Yepez Judith, Campos-Rodríguez Rafael
Department of Experimental Pathology, CINVESTAV-IPN, Av. IPN No.2508 Zacatenco, CP07360, Mexico, DF.
Can J Microbiol. 2008 Dec;54(12):1032-42. doi: 10.1139/W08-106.
Although innate and adaptive immunity both play a role in amoebiasis, the mechanisms involved in the elimination of Entamoeba histolytica are poorly understood. To provide more information about the innate immune mechanisms that may confer protection against invasive amoebiasis, we administered inflammatory substances (bacillus Calmette-Guérin, lipopolysaccharide, complete Freund's adjuvant, or mineral oil) into the peritoneum of hamsters. The animals were then challenged with pathogenic trophozoites of E. histolytica and, after 7 days, the protective host response was analysed. We found that the nonspecific inflammatory response induced in the peritoneum was sufficient to prevent liver invasion by E. histolytica. In vitro experiments showed that the killing of trophozoites was mediated by peritoneal macrophages and a protein of 68 kDa with peroxidase activity.
尽管先天性免疫和适应性免疫在阿米巴病中均发挥作用,但参与清除溶组织内阿米巴的机制仍知之甚少。为了提供更多关于可能赋予针对侵袭性阿米巴病保护作用的先天性免疫机制的信息,我们将炎性物质(卡介苗、脂多糖、完全弗氏佐剂或矿物油)注入仓鼠腹腔。然后用溶组织内阿米巴的致病滋养体对动物进行攻击,并在7天后分析宿主的保护性反应。我们发现,在腹腔诱导的非特异性炎症反应足以防止溶组织内阿米巴侵袭肝脏。体外实验表明,滋养体的杀伤是由腹腔巨噬细胞和一种具有过氧化物酶活性的68 kDa蛋白介导的。