Selenium (Se) is an essential micronutrient contributing to a strong immune system for the prevention of infections and diseases in humans and animals. Dietary Se regulates the immune status and mediates anti-inflammatory action. Mastitis is an inflammation in the mammary gland typically induced through the major pathogen S. aureus. The aim of the present study was to determine the regulating effect of Se on S. aureus-induced inflammation using a mouse mastitis model. Immunofluorescence staining was used to detect histopathological injury. ELISA was used to detect cytokine expression, while protein and mRNA levels were analyzed through Western blotting and qPCR analysis, respectively. The results showed that Se deficiency increased inflammatory lesions in individuals with S. aureus infection in the mammary gland. The NO levels showed a significant increase in Se-deficient mice with S. aureus mastitis. Se deficiency accelerated the production of pro-inflammatory factors and reduced IL-10 expression. Furthermore, the results of the present study showed that the regulating effect of Se on S. aureus-induced mastitis was associated with the NF-κB pathway. Indeed, Se deficiency suppressed PPAR-γ activity and promoted NF-κB pathway activation. Thus, Se supplementation could improve the effect on PPAR-γ and NF-κB. These results suggest that Se deficiency could aggravate the inflammatory injury resulting from S. aureus-induced mastitis. Moreover, the results of the present study contribute to the development of new prevention or treatment methods for S. aureus-induced mastitis and other infectious diseases.
Keywords: Inflammation; NF-κB pathway; PPAR-γ; S. aureus mastitis; Selenium.