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米曲霉凝集素通过与结合在肥大细胞上的非特异性 IgE 中的岩藻糖相互作用,诱导过敏样水肿和肥大细胞活化。

Aspergillus oryzae lectin induces anaphylactoid oedema and mast cell activation through its interaction with fucose of mast cell-bound non-specific IgE.

机构信息

Department of Pharmacology, Kobe Pharmaceutical University, Higashinada-ku, Kobe, Hyogo, Japan.

出版信息

Scand J Immunol. 2011 Nov;74(5):445-53. doi: 10.1111/j.1365-3083.2011.02598.x.

Abstract

We investigated whether Aspergillus oryzae lectin (AOL), a fucose-specific lectin, induces anaphylactoid reactions and mast cell activation. The injection of AOL into footpads of mice produced a dose-related acute paw oedema. The AOL-induced oedema was attenuated by predose of histamine H1 receptor blocker or pretreatment of the lectin with fucose before injection and was not observed in SCID and mast cell-deficient WBB6F1-W/Wv mice. These results suggested that the AOL-induced anaphylactoid reaction was mediated by histamine released from mast cells. In addition, the activation of mast cells was seemed to be induced by the crosslinking of IgE on the cell surface following the binding of AOL to fucose residues in IgE. Consistent with the in vivo results, AOL induced the degranulation of the rat mast cell line RBL2H3 sensitized with monoclonal IgE. As AOL induced the increase in intracellular Ca(2+) concentration of IgE-sensitized RBL2H3 cells as well as antigen stimulation, AOL could input signals from FcεRI. The degranulation of IgE-sensitized RBL2H3 cells by AOL was diminished by pretreatment of AOL with fucose. Defucosylated IgE did not induce degranulation of RBL2H3 cells in response to AOL stimulation, in spite of its ability to induce degranulation by antigen stimulation as intact IgE. These results indicated that AOL bound to fucose residue of IgE causing antigen-independent IgE-mediated mast cell activation and anaphylactoid reactions in vitro and in vivo, respectively. AOL bound to human IgE as well as to mouse IgE, suggesting the possible implication of AOL in the allergic response to Aspergillus oryzae in humans.

摘要

我们研究了米曲霉凝集素(AOL)是否会引起过敏样反应和肥大细胞激活。将 AOL 注射到小鼠的脚掌中会导致剂量相关的急性爪肿胀。预先给予组胺 H1 受体阻滞剂或在用 AOL 注射前用岩藻糖预处理该凝集素,可以减轻 AOL 诱导的水肿,并且在 SCID 和缺乏肥大细胞的 WBB6F1-W/Wv 小鼠中观察不到这种现象。这些结果表明 AOL 诱导的过敏样反应是由肥大细胞释放的组胺介导的。此外,AOL 似乎通过与 IgE 上的岩藻糖残基结合,导致细胞表面 IgE 的交联,从而诱导肥大细胞的激活。与体内结果一致,AOL 诱导了用单克隆 IgE 致敏的大鼠肥大细胞系 RBL2H3 的脱颗粒。由于 AOL 诱导 IgE 致敏的 RBL2H3 细胞内 Ca2+浓度增加以及抗原刺激,因此 AOL 可以从 FcεRI 输入信号。用岩藻糖预处理 AOL 可减少 AOL 对 IgE 致敏的 RBL2H3 细胞的脱颗粒作用。去岩藻糖 IgE 尽管能够诱导完整 IgE 所诱导的抗原刺激下的脱颗粒作用,但不能诱导 IgE 致敏的 RBL2H3 细胞对 AOL 刺激的脱颗粒作用。这些结果表明,AOL 与 IgE 的岩藻糖残基结合,导致体外和体内抗原非依赖性 IgE 介导的肥大细胞激活和过敏样反应。AOL 与人类 IgE 以及小鼠 IgE 结合,表明 AOL 可能参与了人类对米曲霉的过敏反应。

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