Selenium Deficiency Facilitates Inflammation Following S . aureus Infection by Regulating TLR2-Related Pathways in the Mouse Mammary Gland

Abstract

Selenium (Se) is an essential micronutrient affecting various aspects of health. Se deficiency has been associated with inflammation and immune responses. Mastitis poses a serious problem for humans and animals in the postpartum period. Staphylococcus aureus (S. aureus) is the most common infectious bacterial pathogen associated with mastitis. The present study sought to determine the effects and underlying mechanism of dietary Se on S. aureus-induced inflammation using a model of mouse mastitis. ELISA and Western blotting were performed to detect protein levels. Quantitative PCR (qPCR) was performed to detect messenger RNA (mRNA) levels. The histopathological changes indicated that Se deficiency resulted in increased inflammatory lesions in S. aureus mastitis, whereas Se deficiency did not induce inflammatory lesions in the mammary gland. Myeloperoxidase (MPO) activity was increased in Se-deficient mice with S. aureus mastitis. Analysis of cytokine mRNA and protein showed that Se deficiency leads to increased TNF-α, IL-1β, and IL-6 production in S. aureus mastitis. In addition, Se deficiency enhanced the mRNA and protein expressions of toll-like receptor 2 (TLR2), which were originally upregulated by S. aureus in the mammary gland tissues and human embryonic kidney 293 (HEK293)-mTLR2 cells. When Se-deficient mice were infected with S. aureus, the phosphorylation of IκB, nuclear factor-κB (NF-κB), extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 was greatly increased. The results indicate that Se deficiency could intensify the inflammatory reaction in S. aureus mastitis. This work contributes to the exploration of new methods of preventing or treating of S. aureus mastitis and other infectious diseases.

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