Igarashi Kento, Matsunaga Ryohei, Hirakawa Sachi, Hosoya Sho, Suetake Hiroaki, Kikuchi Kiyoshi, Suzuki Yuzuru, Nakamura Osamu, Miyadai Toshiaki, Tasumi Satoshi, Tsutsui Shigeyuki
School of Marine Biosciences, Kitasato University, Kanagawa 252-0373, Japan.
Fisheries Laboratory, The University of Tokyo, Shizuoka 431-0214, Japan; and.
J Immunol. 2017 May 15;198(10):4107-4114. doi: 10.4049/jimmunol.1601996. Epub 2017 Apr 12.
How parasites recognize their definitive hosts is a mystery; however, parasitism is reportedly initiated by recognition of certain molecules on host surfaces. Fish ectoparasites make initial contact with their hosts at body surfaces, such as skin and gills, which are covered with mucosa that are similar to those of mammalian guts. Fish are among the most primitive vertebrates with immune systems that are equivalent to those in mammals, and they produce and secrete IgM into mucus. In this study, we showed that the monogenean parasite utilizes IgM to recognize its host, fugu Oncomiracidia are infective larvae of that shed their cilia and metamorphose into juveniles when exposed to purified d-mannose-binding fractions from fugu mucus. Using liquid chromatography-tandem mass spectrometry analysis, proteins contained in the fraction were identified as d-mannose-specific IgM with two d-mannose-binding lectins. However, although deciliation was significantly induced by IgM and was inhibited by d-mannose or a specific Ab against fugu IgM, other lectins had no effect, and IgM without d-mannose affinity induced deciliation to a limited degree. Subsequent immunofluorescent staining experiments showed that fugu d-mannose-specific IgM binds ciliated epidermal cells of oncomiracidium. These observations suggest that deciliation is triggered by binding of fugu IgM to cell surface Ags via Ag binding sites. Moreover, concentrations of d-mannose-binding IgM in gill mucus were sufficient to induce deciliation in vitro, indicating that parasites initially use host Abs to colonize host gills.
寄生虫如何识别其终末宿主仍是一个谜；然而，据报道，寄生现象是由识别宿主表面的某些分子引发的。鱼类体外寄生虫最初在体表与宿主接触，如皮肤和鳃，这些部位覆盖着类似于哺乳动物肠道的黏膜。鱼类是最原始的脊椎动物之一，其免疫系统与哺乳动物相当，它们会产生并将免疫球蛋白M（IgM）分泌到黏液中。在本研究中，我们表明单殖吸虫寄生虫利用IgM来识别其宿主——河豚。纤毛幼虫是单殖吸虫的感染性幼虫，当暴露于河豚黏液中纯化的d - 甘露糖结合组分时，它们会脱落纤毛并变态为幼虫。通过液相色谱 - 串联质谱分析，该组分中含有的蛋白质被鉴定为具有两种d - 甘露糖结合凝集素的d - 甘露糖特异性IgM。然而，尽管IgM能显著诱导纤毛脱落，且d - 甘露糖或抗河豚IgM的特异性抗体可抑制纤毛脱落，但其他凝集素无此作用，且无d - 甘露糖亲和力的IgM仅能在有限程度上诱导纤毛脱落。随后的免疫荧光染色实验表明，河豚d - 甘露糖特异性IgM与纤毛幼虫的表皮细胞结合。这些观察结果表明，纤毛脱落是由河豚IgM通过抗原结合位点与细胞表面抗原结合触发的。此外，鳃黏液中d - 甘露糖结合IgM的浓度足以在体外诱导纤毛脱落，这表明寄生虫最初利用宿主抗体在宿主鳃上定殖。
