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Published on: March 2, 2019
Impact of Selenium Deficiency on Inflammation, Oxidative Stress, and Phagocytosis in Mouse Macrophages
Jianwen Xu1, Yafan Gong1, Yue Sun1
1College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, People's Republic of China.
Abstract:
Although it has been reported that selenium (Se) deficiency can trigger inflammation, however, there are few reports on the effect of Se on the function of mouse peritoneal macrophages. Herein, we examined the expression of inflammatory factors, oxidative stress levels, and phagocytosis for primary-cultured peritoneal macrophages using control and Se-deficient groups. Our results revealed that Se deficiency induced the accumulation of oxygen free radicals and weakened antioxidant capacity. Se deficiency also significantly increased the expression of inflammation factors including iNOS, IL-1β, IL-12, IL-10, PTGe, and NF-κB. Meanwhile, Se suppression restrained macrophage production of TNF-α. The results of the phagocytosis assay demonstrated that Se deficiency inhibited the phagocytosis of macrophages. In conclusion, Se-deficient macrophages undergo severe inflammation through the NF-κB pathway due to the accumulation of oxygen free radicals and are hindered in their phagocytic capacity.
Insights
Selenium deficiency causes severe inflammation and impairs macrophage function. This study reveals that selenium deficiency leads to increased oxidative stress and inflammation, hindering macrophage phagocytosis via the NF-κB pathway.
Area of Science:
- Immunology
- Nutritional Science
- Cell Biology
Background:
- Selenium (Se) is crucial for immune function.
- Se deficiency is linked to inflammation, but its impact on macrophage function is under-researched.
Purpose of the Study:
- To investigate the effects of Se deficiency on mouse peritoneal macrophage function.
- To analyze inflammatory factor expression, oxidative stress, and phagocytosis in Se-deficient macrophages.
Main Methods:
- Primary culture of mouse peritoneal macrophages from control and Se-deficient groups.
- Measurement of inflammatory factors (iNOS, IL-1β, IL-12, IL-10, PTGe, NF-κB, TNF-α).
- Assessment of oxidative stress (oxygen free radicals) and antioxidant capacity.
- Phagocytosis assays were performed.
Main Results:
- Se deficiency increased oxygen free radical accumulation and reduced antioxidant capacity.
- Expression of iNOS, IL-1β, IL-12, IL-10, PTGe, and NF-κB was significantly elevated.
- Tumor necrosis factor-alpha (TNF-α) production was suppressed.
- Macrophage phagocytic capacity was significantly inhibited.
Conclusions:
- Se deficiency induces severe inflammation in macrophages, mediated by the NF-κB pathway.
- Accumulation of oxygen free radicals contributes to inflammation and impaired phagocytosis in Se-deficient macrophages.
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