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Selenium Ameliorates S. aureus-Induced Inflammation in Bovine Mammary Epithelial Cells by Regulating ROS-Induced NLRP3 Inflammasome

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Abstract

In this study, the regulation effects of selenium (Se) on the expression of pyrin domain-containing protein (NLRP) 3 inflammasome and reactive oxygen species (ROS) in bovine mammary epithelial cells (bMECs) infected by Staphylococcus aureus (S. aureus) were detected. bMECs were treated with 8 μmol/L Na2SeO3 for 12 h before infection with S. aureus for 2 h. Through flow cytometry, Western blot, and qRT-PCR analysis, the expression of ROS and NLRP3 imflammasome was detected. Results showed Se significantly reduced the ROS level in bMECs; at the same time, the expressions of NLRP3, ASC, caspase-1, Pro-IL-1β, and IL-1β were also decreased. In conclusion, Se inhibits S. aureus-induced inflammation by suppressing the activation of NLRP3 inflammasome and ROS in bMECs.

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All data used during the study appear in the submitted article.

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Funding

This work was supported by the National Natural Science Foundation (NO. 31802254) of China; the Science and Technology Project of Shandong Province higher education institutions (NO. J18KB074); and the Key Research and Development Project of Hebei (19226625D).

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Yan Yang and Zhennan Wang contributed to the overall study design and supervised all research. Junjun Liu analyzed the data and prepared figures and contributed partly to writing and finally revising the manuscript and data analysis. Shenjin Lv drafted and revised the first version of the manuscript. All the authors reviewed and finally approved the manuscript.

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Correspondence to Zhennan Wang or Junjun Liu.

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All experimental procedures were conducted with the approval of the Institutional Animal Care and Use Committee of Linyi University.

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The authors declare no competing interests.

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Yang, Y., Lv, S., Wang, Z. et al. Selenium Ameliorates S. aureus-Induced Inflammation in Bovine Mammary Epithelial Cells by Regulating ROS-Induced NLRP3 Inflammasome. Biol Trace Elem Res 200, 3171–3175 (2022). https://doi.org/10.1007/s12011-021-02924-7

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  • DOI: https://doi.org/10.1007/s12011-021-02924-7

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