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肥大细胞对甲醛的反应。1. 介质释放的调节。

Mast cell response to formaldehyde. 1. Modulation of mediator release.

作者信息

Fujimaki H, Kawagoe A, Bissonnette E, Befus D

机构信息

Division of Environmental Health Sciences, National Institute for Environmental Studies, Ibaraki, Japan.

出版信息

Int Arch Allergy Immunol. 1992;98(4):324-31. doi: 10.1159/000236206.

DOI:10.1159/000236206
PMID:1384864
Abstract

To examine the effects of the atmospheric pollutant formaldehyde on functionally distinct mast cells, peritoneal mast cells (PMC), intestinal mucosal mast cells (IMMC) and mouse bone-marrow-derived mast cells (BMMC) were incubated with various concentrations of formaldehyde. Pretreatment for 30 min with up to 100 micrograms/ml formaldehyde was not cytotoxic to mast cells. Formaldehyde (1-10 micrograms/ml) alone induced low levels of histamine release (< 10%) from IMMC and BMMC. Antigen-induced histamine release was significantly increased in both PMC pretreated with low concentrations of formaldehyde (5-20 micrograms/ml) and BMMC pretreated with 10 micrograms/ml formaldehyde but decreased in PMC pretreated with a higher concentration (100 micrograms/ml) of formaldehyde. By contrast, antigen-induced histamine release was decreased in IMMC pretreated with formaldehyde in a dose-dependent manner. Histamine release stimulated with A23187 was also increased in PMC pretreated with a low concentration (10 micrograms/ml) of formaldehyde but decreased in those pretreated with a higher concentration (100 micrograms/ml) of formaldehyde. Pretreatment with 10 micrograms/ml formaldehyde significantly enhanced beta-hexosaminidase release from PMC stimulated with antigen or A23187. Compared to sham-treated PMC, PMC pretreated with formaldehyde expressed a markedly depressed natural cytotoxicity for the tumor target WEHI-164 (an assay of tumor necrosis factor alpha activity). These results suggest that formaldehyde modifies various mast cell functions through alterations in cellular metabolism. Such effects may be important in respiratory and other diseases associated with formaldehyde exposure.

摘要

为研究大气污染物甲醛对功能不同的肥大细胞的影响,将腹膜肥大细胞(PMC)、肠黏膜肥大细胞(IMMC)和小鼠骨髓来源的肥大细胞(BMMC)与不同浓度的甲醛一起孵育。用高达100微克/毫升的甲醛预处理30分钟对肥大细胞无细胞毒性。单独使用甲醛(1 - 10微克/毫升)可诱导IMMC和BMMC释放低水平的组胺(<10%)。在低浓度甲醛(5 - 20微克/毫升)预处理的PMC和10微克/毫升甲醛预处理的BMMC中,抗原诱导的组胺释放均显著增加,但在高浓度(100微克/毫升)甲醛预处理的PMC中则降低。相比之下,甲醛预处理的IMMC中抗原诱导的组胺释放呈剂量依赖性降低。用低浓度(10微克/毫升)甲醛预处理的PMC中,A23187刺激的组胺释放也增加,但在高浓度(100微克/毫升)甲醛预处理的PMC中则降低。用10微克/毫升甲醛预处理可显著增强抗原或A23187刺激的PMC中β - 己糖胺酶的释放。与假处理的PMC相比,甲醛预处理的PMC对肿瘤靶标WEHI - 164(肿瘤坏死因子α活性测定)的天然细胞毒性明显降低。这些结果表明,甲醛通过改变细胞代谢来调节肥大细胞的多种功能。这种作用在与甲醛暴露相关的呼吸道疾病和其他疾病中可能很重要。

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PLoS One. 2015 Nov 16;10(11):e0142816. doi: 10.1371/journal.pone.0142816. eCollection 2015.