Aspergillus oryzae Lectin Induces Anaphylactoid Oedema and Mast Cell Activation Through its Interaction With Fucose of Mast Cell–Bound Non‐specific IgE
Aspergillus oryzae Lectin Induces Anaphylactoid Oedema and Mast Cell Activation Through its Interaction With Fucose of Mast Cell–Bound Non‐specific IgE
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米曲霉凝集素通过与肥大细胞结合的非特异性 IgE 的岩藻糖相互作用诱导过敏性水肿和肥大细胞活化
DOI：
10.1111/j.1365-3083.2011.02598.x
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发表时间：
2011
影响因子：
3.7
通讯作者：
S. Yoshino
中科院分区：
文献类型：
--
作者：
K. Yamaki;S. Yoshino
我们研究了曲霉菌凝集素（AOL）（一种岩藻糖特异性凝集素）是否诱导过敏样反应和肥大细胞活化。将AOL注射到小鼠足垫中产生了剂量相关的急性爪水肿。注射前给予组胺H1受体阻滞剂或用岩藻糖预处理凝集素可减轻AOL诱导的水肿，在SCID和肥大细胞缺陷型WBB 6 F1-W/Wv小鼠中未观察到。这些结果表明AOL诱导的类速发过敏反应由肥大细胞释放的组胺介导。此外，肥大细胞的活化似乎是由IgE在细胞表面上的交联诱导的，随后AOL与IgE中的岩藻糖残基结合。与体内结果一致，AOL诱导用单克隆IgE致敏的大鼠肥大细胞系RBL 2 H3的脱粒。由于AOL诱导IgE致敏的RBL 2 H3细胞内Ca 2+浓度增加以及抗原刺激，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RBL 2 H3细胞的脱粒作用。去岩藻糖基化IgE不诱导RBL 2 H3细胞对AOL刺激的脱粒，尽管其能够通过抗原刺激诱导脱粒作为完整的IgE。这些结果表明AOL与IgE的岩藻糖残基结合，分别在体外和体内引起抗原非依赖性IgE介导的肥大细胞活化和类速发过敏反应。AOL与人IgE以及小鼠IgE结合，表明AOL可能与人类对曲霉菌的过敏反应有关。
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 Ca2+ 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.
影响因子：
14.2
作者：
Stone, Kelly D.;Prussin, Calman;Metcalfe, Dean D.
通讯作者：
Metcalfe, Dean D.
DOI：
10.1016/s0021-9258(18)83166-0
发表时间：
1989-05
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
J P Y Kao;A. Harootunian;R. Tsien
通讯作者：
J P Y Kao;A. Harootunian;R. Tsien
莫能菌素存在时分泌的人纤连蛋白糖基化异常。
DOI：
--
发表时间：
1983
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Ledger,PW;Nishimoto,SK;Hayashi,S;Tanzer,ML
通讯作者：
Tanzer,ML