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肥大细胞脱颗粒产物在肥大细胞增生中的作用。I. 神经生长因子的作用机制。

The role of mast cell degranulation products in mast cell hyperplasia. I. Mechanism of action of nerve growth factor.

作者信息

Marshall J S, Stead R H, McSharry C, Nielsen L, Bienenstock J

机构信息

Department of Pathology and Molecular Virology, McMaster University, Hamilton, Ontario, Canada.

出版信息

J Immunol. 1990 Mar 1;144(5):1886-92.

PMID:2106555
Abstract

A variety of mast cell degranulating agents have previously been shown to induce mast cell hyperplasia in adult rats. In neonates 2.5 S nerve growth factor (NGF) induces a hyperplasia of both mucosal and connective tissue mast cells (MMC and CTMC). We have examined the role of the potent mast cell degranulating properties of NGF on its ability to induce mast cell hyperplasia. Administration of NGF in combination with the mast cell stabilizing agent disodium cromoglycate was found to abrogate the CTMC hyperplasia induced by NGF alone. Treatment of neonatal rats with the alternate degranulating agent compound 48/80 was found to induce a limited CTMC but not a MMC hyperplasia. A supernatant obtained by degranulating purified adult rat peritoneal mast cells with anti-IgE was found to induce hyperplasia of the CTMC population similar to that observed with NGF administration. However, this degranulation product supernatant only induced a limited MMC hyperplasia as judged by RMCP II content of the tissues. These results suggest that NGF has dual action inducing mast cell hyperplasia; CTMC hyperplasia being dependent on the ability of NGF to degranulate mast cells. MMC hyperplasia induced by NGF is independent of CTMC degranulation. Degranulation products from peritoneal mast cells act to increase both MMC and CTMC populations in the neonate. These data suggest that the CTMC population may be regulated by an autocrine positive feedback mechanism in vivo.

摘要

此前已表明,多种肥大细胞脱颗粒剂可诱导成年大鼠肥大细胞增生。在新生大鼠中,2.5S神经生长因子(NGF)可诱导黏膜和结缔组织肥大细胞(MMC和CTMC)增生。我们研究了NGF强大的肥大细胞脱颗粒特性在其诱导肥大细胞增生能力中的作用。发现将NGF与肥大细胞稳定剂色甘酸钠联合给药可消除单独使用NGF诱导的CTMC增生。发现用替代脱颗粒剂化合物48/80处理新生大鼠可诱导有限的CTMC增生,但不会诱导MMC增生。用抗IgE使纯化的成年大鼠腹膜肥大细胞脱颗粒获得的上清液可诱导CTMC群体增生,类似于给予NGF时观察到的情况。然而,根据组织中RMCP II含量判断,这种脱颗粒产物上清液仅诱导有限的MMC增生。这些结果表明,NGF具有诱导肥大细胞增生的双重作用;CTMC增生依赖于NGF使肥大细胞脱颗粒的能力。NGF诱导的MMC增生与CTMC脱颗粒无关。腹膜肥大细胞的脱颗粒产物可增加新生大鼠的MMC和CTMC群体。这些数据表明,CTMC群体在体内可能受自分泌正反馈机制调节。

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