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暴露于镉的小鼠对病毒诱导的心肌炎的免疫反应和抵抗力

Immune responses and resistance to viral-induced myocarditis in mice exposed to cadmium.

作者信息

Ilbäck N G, Fohlman J, Friman G, Ehrnst A

机构信息

Kabi Pharmacia AB, Helsingborg, Sweden.

出版信息

Chemosphere. 1994 Sep;29(6):1145-54. doi: 10.1016/0045-6535(94)90251-8.

DOI:10.1016/0045-6535(94)90251-8
PMID:7953467
Abstract

The effects of 10 weeks of treatment with cadmium (Cd) on the immune function and resistance to coxsackievirus B3 (CB3)-induced myocarditis in female Balb/c mice were investigated. A 2mM dose of Cd in the drinking water did not influence mortality due to the CB3 infection. The inflammatory and necrotic lesions in the ventricular myocardium seven days after inoculation (2.94% of tissue section area) were not increased by Cd (2.82% of tissue section area). The response pattern of lymphocyte subsets in situ in myocardial inflammatory lesions was elucidated by an immune histochemical staining technique. With Cd treatment the number of cytotoxic T cells and B cells in these lesions decreased by 22% (n.s.) and 21% (p < 0.05), respectively. Spleen weight and the lymphoproliferative response to the B-lymphocyte mitogen increased by 19% (p < 0.05) and 23% (n.s.), respectively. The titers of neutralizing antibodies increased by 22% (n.s.) with Cd treatment. However, the activity of spleen T lymphocytes and spontaneous cell-mediated cytotoxicity (NK-cell) was unchanged. Thymus weight and WBC count in peripheral blood tended to decrease. Thus, Cd exposure seems to result in a decreased maturation and mobilization of T and B lymphocytes, but increased humoral immune host responses.

摘要

研究了用镉(Cd)对雌性Balb/c小鼠进行10周治疗对其免疫功能及抗柯萨奇病毒B3(CB3)诱导的心肌炎抵抗力的影响。饮用水中2mM剂量的Cd不影响因CB3感染导致的死亡率。接种七天后,心室心肌中的炎症和坏死病变(占组织切片面积的2.94%)并未因Cd(占组织切片面积的2.82%)而增加。采用免疫组织化学染色技术阐明了心肌炎性病变中原位淋巴细胞亚群的反应模式。经Cd治疗后,这些病变中细胞毒性T细胞和B细胞的数量分别减少了22%(无统计学意义)和21%(p<0.05)。脾脏重量和对B淋巴细胞有丝分裂原的淋巴细胞增殖反应分别增加了19%(p<0.05)和23%(无统计学意义)。经Cd治疗后,中和抗体滴度增加了22%(无统计学意义)。然而,脾脏T淋巴细胞的活性和自发细胞介导的细胞毒性(NK细胞)未发生变化。胸腺重量和外周血白细胞计数有下降趋势。因此,接触Cd似乎会导致T和B淋巴细胞的成熟和动员减少,但会增强体液免疫宿主反应。

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