Allicin Alleviated LPS-Induced Mastitis via the TLR4/NF-κB Signaling Pathway in Bovine Mammary Epithelial Cells

Abstract

Dairy farming is the most important economic activity in animal husbandry. Mastitis is the most common disease in dairy cattle and has a significant impact on milk quality and yield. The natural extract allicin, which is the main active ingredient of the sulfur-containing organic compounds in garlic, has anti-inflammatory, anticancer, antioxidant, and antibacterial properties; however, the specific mechanism underlying its effect on mastitis in dairy cows needs to be determined. Therefore, in this study, whether allicin can reduce lipopolysaccharide (LPS)-induced inflammation in the mammary epithelium of dairy cows was investigated. A cellular model of mammary inflammation was established by pretreating bovine mammary epithelial cells (MAC-T) with 10 µg/mL LPS, and the cultures were then treated with varying concentrations of allicin (0, 1, 2.5, 5, and 7.5 µM) added to the culture medium. MAC-T cells were examined using RT–qPCR and Western blotting to determine the effect of allicin. Subsequently, the level of phosphorylated nuclear factor kappa-B (NF-κB) was measured to further explore the mechanism underlying the effect of allicin on bovine mammary epithelial cell inflammation. Treatment with 2.5 µM allicin considerably decreased the LPS-induced increase in the levels of the inflammatory cytokines interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-α (TNF-α) and inhibited activation of the NOD-like receptor protein 3 (NLRP3) inflammasome in cow mammary epithelial cells. Further research revealed that allicin also inhibited the phosphorylation of inhibitors of nuclear factor kappa-B-α (IκB-α) and NF-κB p65. In mice, LPS-induced mastitis was also ameliorated by allicin. Therefore, we hypothesize that allicin alleviated LPS-induced inflammation in the mammary epithelial cells of cows probably by affecting the TLR4/NF-κB signaling pathway. Allicin will likely become an alternative to antibiotics for the treatment of mastitis in cows.

Saikosaponin A alleviates Staphylococcus aureus‐induced mastitis in mice by inhibiting ferroptosis via SIRT1/Nrf2 pathway

“…IL‐1β is produced in the early stages of infection and is thought to be an important mediator of inflammation 36 . TNF‐α is a pluripotent and proinflammatory cytokine produced by activated macrophages, and TNF‐α induces the production of other cytokines, such as IL‐6, during infection, thereby increasing leukocyte accumulation and amplifying the inflammatory cascade 37,38 . However, these cytokines can also induce overactivation of neutrophils in tissues, which in turn exacerbates disease process in the host 39 .…”

“…36 TNFα is a pluripotent and proinflammatory cytokine produced by activated macrophages, and TNFα induces the production of other cytokines, such as IL-6, during infection, thereby increasing leukocyte accumulation and amplifying the inflammatory cascade. 37,38 However, these cytokines can also induce overactivation of neutrophils in tissues, which in turn exacerbates disease process in the host. 39 The data herein showed that TNFα, IL-1β, neutrophil infiltration and pathological damage were increased in mammary gland.…”

Isolation and Whole Genome Sequence Analysis of Cow Mastitis Candida tropicalis

“…This infectious disease not only adversely affects the milk quality and production performance of dairy cows but also results in signi cant economic losses for the dairy industry [1][2][3] . Microbial invasion, the main cause of mastitis, is mainly caused by bacteria, but in recent studies fungal, viral and mycoplasma infections are also on the rise [4,5] . In the case of mammary gland fungal infection, yeasts of the genus Candida are the most frequently reported fungal pathogens in dairy cow mastitis [6] .…”

Allicin Inhibits Porcine Reproductive and Respiratory Syndrome Virus Infection In Vitro and Alleviates Inflammatory Responses

“…Similarly, allicin exerts an antiviral effect against the reticuloendotheliosis virus by restricting inflammation and oxidative damage caused by the infection, especially by blocking the ERK/MAPK pathway [ 20 ]. Inhibition of the P38 and JNK pathways and the TLR4/NF- κ B signaling pathway was also considered as the anti-inflammatory mechanism of allicin [ 14 , 21 ].…”