Queensland Tropical Health Alliance and School of Public Health and Tropical Medicine, James Cook University, Cairns, Queensland, Australia.
PLoS Pathog. 2012 Feb;8(2):e1002520. doi: 10.1371/journal.ppat.1002520. Epub 2012 Feb 9.
The mucosal cytokine response of healthy humans to parasitic helminths has never been reported. We investigated the systemic and mucosal cytokine responses to hookworm infection in experimentally infected, previously hookworm naive individuals from non-endemic areas. We collected both peripheral blood and duodenal biopsies to assess the systemic immune response, as well as the response at the site of adult worm establishment. Our results show that experimental hookworm infection leads to a strong systemic and mucosal Th2 (IL-4, IL-5, IL-9 and IL-13) and regulatory (IL-10 and TGF-β) response, with some evidence of a Th1 (IFN-γ and IL-2) response. Despite upregulation after patency of both IL-15 and ALDH1A2, a known Th17-inducing combination in inflammatory diseases, we saw no evidence of a Th17 (IL-17) response. Moreover, we observed strong suppression of mucosal IL-23 and upregulation of IL-22 during established hookworm infection, suggesting a potential mechanism by which Th17 responses are suppressed, and highlighting the potential that hookworms and their secreted proteins offer as therapeutics for human inflammatory diseases.
健康人类对寄生虫蠕虫的黏膜细胞因子反应从未被报道过。我们研究了来自非流行地区的实验性感染、先前未感染钩虫的个体对钩虫感染的全身和黏膜细胞因子反应。我们收集外周血和十二指肠活检样本,以评估全身免疫反应以及成虫定植部位的反应。我们的结果表明,实验性钩虫感染导致强烈的全身和黏膜 Th2(IL-4、IL-5、IL-9 和 IL-13)和调节性(IL-10 和 TGF-β)反应,有一些 Th1(IFN-γ 和 IL-2)反应的证据。尽管在成虫通行后 IL-15 和 ALDH1A2 的上调,这是炎症性疾病中已知的 Th17 诱导组合,但我们没有看到 Th17(IL-17)反应的证据。此外,我们观察到在建立的钩虫感染期间,黏膜 IL-23 强烈抑制和 IL-22 上调,这表明了 Th17 反应受到抑制的潜在机制,并强调了钩虫及其分泌蛋白作为人类炎症性疾病治疗方法的潜力。