Chu Daniel, Bungiro Richard D, Ibanez Maureen, Harrison Lisa M, Campodonico Eva, Jones Brian F, Mieszczanek Juliusz, Kuzmic Petr, Cappello Michael
Child Health Research Center, Department of Pediatrics, Yale School of Medicine, New Haven, Connecticut 06520-8081, USA.
Infect Immun. 2004 Apr;72(4):2214-21. doi: 10.1128/IAI.72.4.2214-2221.2004.
Hookworm infection is a major cause of iron deficiency anemia and malnutrition in developing countries. The Ancylostoma ceylanicum Kunitz-type inhibitor (AceKI) is a 7.9-kDa broad-spectrum inhibitor of trypsin, chymotrypsin, and pancreatic elastase that has previously been isolated from adult hookworms. Site-directed mutagenesis of the predicted P1 inhibitory reactive site amino acid confirmed the role of Met(26) in mediating inhibition of the three target serine proteases. By using reverse transcription-PCR, it was demonstrated that the level of AceKI gene expression increased following activation of third-stage larvae with serum and that the highest level of expression was reached in the adult stage of the parasite. Immunohistochemistry studies performed with polyclonal immunoglobulin G raised against recombinant AceKI showed that the inhibitor localized to the subcuticle of the adult hookworm, suggesting that it has a potential in vivo role in neutralizing intestinal proteases at the surface of the parasite. Immunization with recombinant AceKI was shown to confer partial protection against hookworm-associated growth delay without a measurable effect on anemia. Taken together, the data suggest that AceKI plays a role in the pathogenesis of hookworm-associated malnutrition and growth delay, perhaps through inhibition of nutrient absorption in infected hosts.
钩虫感染是发展中国家缺铁性贫血和营养不良的主要原因。锡兰钩虫库尼茨型抑制剂(AceKI)是一种7.9 kDa的胰蛋白酶、糜蛋白酶和胰弹性蛋白酶的广谱抑制剂,此前已从成年钩虫中分离出来。对预测的P1抑制反应位点氨基酸进行定点诱变,证实了Met(26)在介导对三种靶标丝氨酸蛋白酶的抑制中的作用。通过逆转录PCR表明,用血清激活三期幼虫后,AceKI基因表达水平升高,并且在寄生虫的成虫阶段达到最高表达水平。用针对重组AceKI产生的多克隆免疫球蛋白G进行的免疫组织化学研究表明,该抑制剂定位于成年钩虫的皮下,这表明它在体内可能具有中和寄生虫表面肠道蛋白酶的作用。用重组AceKI免疫显示可对钩虫相关的生长迟缓提供部分保护,而对贫血没有可测量的影响。综上所述,数据表明AceKI可能通过抑制受感染宿主的营养吸收,在钩虫相关营养不良和生长迟缓的发病机制中发挥作用。