Cooperative Wildlife Research Laboratory, Southern Illinois University, Carbondale, Illinois, USA.
Environ Toxicol Chem. 2011 Jun;30(6):1328-37. doi: 10.1002/etc.519. Epub 2011 Apr 4.
This study evaluated the effects of dietary methylmercury (MeHg) on immune system development in captive-reared nestling American kestrels (Falco sparverius) to determine whether T cell-mediated and antibody-mediated adaptive immunity are targets for MeHg toxicity at environmentally relevant concentrations. Nestlings received various diets, including 0 (control), 0.6, and 3.9 µg/g (dry wt) MeHg for up to 18 d posthatch. Immunotoxicity endpoints included cell-mediated immunity (CMI) using the phytohemagglutinin (PHA) skin-swelling assay and antibody-mediated immune response via the sheep red blood cell (SRBC) hemagglutination assay. T cell- and B cell-dependent histological parameters in the spleen, thymus, and bursa of Fabricius were correlated with the functional assays. For nestlings in the 0.6 and 3.9 µg/g MeHg groups, CMI was suppressed by 73 and 62%, respectively, at 11 d of age. Results of this functional assay were correlated with T cell-dependent components of the spleen and thymus. Dose-dependent lymphoid depletion in spleen tissue directly affected the proliferation of T-lymphocyte populations, insofar as lower stimulation indexes from the PHA assay occurred in nestlings with lower proportions of splenic white pulp and higher THg concentrations. Nestlings in the 3.9 µg/g group also exhibited lymphoid depletion and a lack of macrophage activity in the thymus. Methylmercury did not have a noticeable effect on antibody-mediated immune function or B cell-dependent histological correlates. We conclude that T cell-mediated immunosuppression is the primary target of MeHg toward adaptive immunity in developing kestrels. This study provides evidence that environmentally relevant concentrations of MeHg may compromise immunocompetence in a developing terrestrial predator and raises concern regarding the long-term health effects of kestrels that were exposed to dietary MeHg during early avian development.
本研究评估了饮食甲基汞(MeHg)对圈养育雏期美洲红隼(Falco sparverius)免疫系统发育的影响,以确定 T 细胞介导和抗体介导的适应性免疫是否是环境相关浓度下 MeHg 毒性的靶标。雏鸟接受了不同的饮食,包括 0(对照)、0.6 和 3.9μg/g(干重)的 MeHg,直至孵化后 18 天。免疫毒性终点包括使用植物血凝素(PHA)皮肤肿胀测定法进行细胞介导的免疫(CMI)和通过绵羊红细胞(SRBC)血凝测定法进行抗体介导的免疫反应。脾、胸腺和法氏囊的 T 细胞和 B 细胞依赖性组织学参数与功能测定相关。在 0.6 和 3.9μg/g MeHg 组的雏鸟中,分别在 11 日龄时 CMI 受到 73%和 62%的抑制。该功能测定的结果与脾和胸腺的 T 细胞依赖性成分相关。脾组织中淋巴细胞的剂量依赖性耗竭直接影响 T 淋巴细胞群体的增殖,因为 PHA 测定中的较低刺激指数发生在脾白髓比例较低和 THg 浓度较高的雏鸟中。3.9μg/g 组的雏鸟还表现出胸腺中的淋巴细胞耗竭和巨噬细胞活性缺乏。MeHg 对抗体介导的免疫功能或 B 细胞依赖性组织学相关性没有明显影响。我们得出结论,T 细胞介导的免疫抑制是 MeHg 对发育中红隼适应性免疫的主要靶标。本研究提供了证据表明,环境相关浓度的 MeHg 可能会损害正在发育的陆地捕食者的免疫能力,并对在早期鸟类发育过程中暴露于饮食 MeHg 的红隼的长期健康影响表示关注。