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Mastitis, a major disease affecting dairy cows, is most commonly caused by Staphylococcus aureus (S. aureus). Selenium (Se) can activate pivotal proteins in immune responses and regulate the immune system, and microRNA-155 (miR-155) is a key transcriptional regulator for inflammation-related diseases. We constructed the model of mouse mastitis in vivo and primary mouse mammary epithelial cells (MMECs) in vitro, which were induced by S. aureus. Se content of the mammary was estimated using an atomic fluorescence spectrophotometer. Histopathological analysis was performed via hematoxylin and eosin (H&E) staining. The mmu-miR-155-5p mimic was transfected in MMECs, and viability was determined through the MTT assay. Transfected efficiency was evaluated by qPCR and fluorescence staining. Cytokines including TNF-α, IL-1β, IL-10 and TLRs were detected with qPCR. In addition, western blotting was used to evaluate the expression of the NF-κB and MAPKs signaling pathways. The results demonstrated that a Se-supplemented diet improved the content of Se in mammary tissues. Histopathological studies indicated that the mammary glands were protected in the Se-supplemented group after S. aureus infection. Se-supplementation suppressed the production of MPO, mmu-miR-155, TNF-α, IL-1β, and TLR2 and significantly inhibited the phosphorylation of NF-κB and MAPKs in vivo and in vitro. All the data indicated that mmu-miR-155 played a pro-inflammatory role in our study, and Se-supplementation could suppress the expression of mmu-miR-155 to inhibit inflammation in S. aureus-induced mastitis in mice.

Mastitis, inflammation of the mammary gland, occurs in both humans and animals. Staphylococcus aureus is the most common infectious bacterial pathogen associated with mastitis. We investigated the effects of allicin on S. aureus -induced mastitis in mice. Pathological histology revealed that allicin inhibited S. aureus -induced pathological damage and myeloperoxidase activity in mammary tissues. Enzyme-linked immunosorbent assays demonstrated that allicin reduced the production of IL-1β and TNF-α as well as inhibited the NF-κB and mitogen-activated protein kinase pathway by reducing phosphorylation of p65, IκBα, p38, JNK, and ERK. Western blotting revealed that allicin reduced TLR2 and TLR6 expression in mammary tissues and cells but not in HEK293 cells. The lipid raft content was reduced by allicin, which inhibited signaling downstream of TLR2 and TLR6. Liver X receptor α ( LXR α) luciferase reporter assays and LXR α interference experiments showed that allicin improved the LXR α activity and adenosine 5'-triphosphate-binding cassette G and A1 (ABCG and ABCA1) expression, thereby reducing the cholesterol level, lipid raft formation, and downstream TLR2 and TLR6 pathway activity. These results demonstrated that allicin exerted anti-inflammatory effects against S. aureus mastitis by improving the LXR α activity and reducing lipid raft formation.

Mastitis is a serious and prevalent disease caused by infection by pathogens such as Staphylococcus aureus. We evaluated the anti-inflammatory effects and mechanism of luteolin, a natural flavonoid with a wide range of pharmacological activities, in a mouse model of S. aureus mastitis. We also treated cultured mouse mammary epithelial cells (mMECs) with S. aureus and luteolin. Histopathological changes were examined by H&E staining and the levels of inflammatory cytokine proteins were analyzed using ELISAs. We determined mRNA levels with qPCR and the level of NF-κB and matrix metalloproteinase (MMP) proteins by Western blotting. The observed histopathological changes showed that luteolin protected mammary glands with S. aureus infection from tissue destruction and inflammatory cell infiltration. Luteolin inhibited the expression of TNF-α, IL-1β, and IL-6, all of which were increased with S. aureus infection of mammary tissues and mMECs. S. aureus-induced TLR2 and TLR4 was suppressed by luteolin, as were levels of IκBα and NF-κB p65 phosphorylation and expression of MMP-2 and MMP-9. Levels of tissue inhibitor of metalloproteinases (TIMP)-1 and TIMP-2 were enhanced. These findings suggest luteolin is a potentially effective new treatment to reduce tissue damage and inflammation from S. aureus-induced mastitis.

Mastitis is a postpartum disease in both humans and animals. Staphylococcus aureus (S. aureus) can induce mastitis by infection of the lactiferous ducts. There is no efficacious treatment for S. aureus-induced mastitis. Betulin has been confirmed to have multiple biological activities, including anti-inflammatory properties. The present study was to determine the anti-inflammatory effect of betulin on S. aureus-induced mastitis and to confirm the mechanism of action involved. In vivo, betulin ameliorated the histopathological changes that were induced by S. aureus. ELISA and qPCR results showed that betulin inhibited TNF-α, IL-1β and IL-6 production. Western blotting results demonstrated that betulin inhibited NF-κB phosphorylation but promoted the expression of PPAR-γ. Further investigations were performed in vitro with mouse Mammary Epithelial Cells (mMECs). The results indicated the betulin inhibited the activity of the NF-κB pathway and increased PPAR-γ expression and transcriptional activity. All of the results in the present study demonstrated that betulin played a protective anti-inflammatory role against S. aureus infection in mammary gland tissues and cells by activating PPAR-γ and inhibiting the activation of NF-κB., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Mastitis, which commonly occurs during the postpartum period, is caused by the infection of the mammary glands. The most common infectious bacterial pathogen of mastitis is Staphylococcus aureus (S. aureus) in both human and animals. Brazilin, a compound isolated from the traditional herbal medicine Caesalpinia sappan L., has been shown to exhibit multiple biological properties. The present study was performed to determine the effect of brazilin on the inflammatory response in the mouse model of S. aureus mastitis and to confirm the mechanism of action involved. Brazilin treatment was applied in both a mouse model and cells. After brazilin treatment of cells, Western blotting and qPCR were performed to detect the protein levels and mRNA levels, respectively. Brazilin treatment significantly attenuated inflammatory cell infiltration and inhibited the expressions of TNF-α, IL-1β and IL-6 in a dose-dependent manner. Administration of brazilin in mice suppressed S. aureus-induced inflammatory injury and the production of proinflammatory mediators. This suppression was achieved by reducing the increased expression of TLR2 and regulating the NF-κB and MAPK signaling pathways in the mammary gland tissues and cells with S. aureus-induced mastitis. These results suggest that brazilin appears to be an effective drug for the treatment of mastitis and may be applied as a clinical therapy., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Mastitis is a major disease in humans and other animals and is characterized by mammary gland inflammation. It is a major disease of the dairy industry. Bergenin is an active constituent of the plants of genus Bergenia. Research indicates that bergenin has multiple biological activities, including anti-inflammatory and immunomodulatory properties. The objective of this study was to evaluate the protective effects and mechanism of bergenin on the mammary glands during lipopolysaccharide (LPS)-induced mastitis. In this study, mice were treated with LPS to induce mammary gland mastitis as a model for the disease. Bergenin treatment was initiated after LPS stimulation for 24 h. The results indicated that bergenin attenuated inflammatory cell infiltration and decreased the concentration of NO, TNF-α, IL-1β, and IL-6, which were increased in LPS-induced mouse mastitis. Furthermore, bergenin downregulated the phosphorylation of nuclear factor-kappaB (NF-κB) and mitogen-activated protein kinases (MAPK) signaling pathway proteins in mammary glands with mastitis. In conclusion, bergenin reduced the expression of NO, TNF-α, IL-1β, and IL-6 proinflammatory cytokines by inhibiting the activation of the NF-κB and MAPKs signaling pathways, and it may represent a novel treatment strategy for mastitis.