Balabekova Marina K, Ostapchuk Yekaterina O, Perfilyeva Yuliya V, Tokusheva Aliya N, Nurmuhambetov Adilman, Tuhvatshin Rustam R, Trubachev Vasiliy V, Akhmetov Zhaugashty B, Abdolla Nurshat, Kairanbayeva Gulgul K, Sulev Koks, Belyaev Nikolai N
Department of Pathological Physiology, S.D. Asfendiyarov Kazakh National Medical University, Almaty, Kazakhstan.
Laboratory of Molecular Immunology and Immunobiotechnology, M.A. Aitkhozhin's Institute of Molecular Biology and Biochemistry, Almaty, Kazakhstan.
Drug Chem Toxicol. 2021 May;44(3):277-285. doi: 10.1080/01480545.2019.1585446. Epub 2019 Mar 8.
Heavy metal pollution is rapidly increasing in the environment. It has been shown that exposure to vanadium and chromium is able to alter the immune response. Nevertheless, the mechanisms by which these metal pollutants mediate their immunomodulatory effects are not completely understood. Herein, we examined the effect of ammonium metavanadate and potassium dichromate on the development of an inflammatory response caused by subcutaneous injection of turpentine oil. We demonstrated that pretreatment of rats with ammonium metavanadate and potassium dichromate for two weeks prior to initiation of the inflammatory response resulted in a wider zone of necrosis surrounding the site of inflammation. The acute inflammatory process in the combined model was characterized by elevated serum levels of IL-10 and decreased serum levels of IL-6 as compared to rats not treated with ammonium metavanadate and potassium dichromate. Ammonium metavanadate and potassium dichromate administration induced a decrease in the proportion of splenic His48CD11b/c myeloid cells accompanied by a reduced infiltration of the wound with neutrophils. Further analysis showed decreased proportions of CD3CD4IFNγ and CD3CD4IL-4 T cells in the rats with combined model as compared to inflamed rats not treated with ammonium metavanadate and potassium dichromate. The data suggest that consumption of vanadium and chromium compounds disrupts the inflammatory response through an altered balance of pro- and anti-inflammatory cytokines and inhibition of effector T cell activation and neutrophil expansion.
环境中的重金属污染正在迅速增加。研究表明，接触钒和铬能够改变免疫反应。然而，这些金属污染物介导其免疫调节作用的机制尚未完全明确。在此，我们研究了偏钒酸铵和重铬酸钾对皮下注射松节油引起的炎症反应发展的影响。我们证明，在炎症反应开始前两周用偏钒酸铵和重铬酸钾预处理大鼠，会导致炎症部位周围出现更广泛的坏死区域。与未用偏钒酸铵和重铬酸钾处理的大鼠相比，联合模型中的急性炎症过程表现为血清白细胞介素-10水平升高和血清白细胞介素-6水平降低。给予偏钒酸铵和重铬酸钾导致脾脏His48CD11b/c髓样细胞比例下降，同时伤口处中性粒细胞浸润减少。进一步分析表明，与未用偏钒酸铵和重铬酸钾处理的炎症大鼠相比，联合模型大鼠中CD3CD4IFNγ和CD3CD4IL-4 T细胞的比例降低。数据表明，钒和铬化合物的摄入通过改变促炎和抗炎细胞因子的平衡以及抑制效应T细胞活化和中性粒细胞扩增来破坏炎症反应。
