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Mastitis has been recognized as a common and major disease of cows with a strong impact on dairy farming. Interleukin-17A (IL-17A) has been shown to mediate crucial crosstalk between the immune system and various epithelial tissues, initiating a series of defensive mechanisms against bacterial and fungal infections. This crosstalk is especially involved in neutrophil infiltration. To evaluate the role of IL-17A in immune defense in the mammary gland in mice, we tested the effects of depleting IL-17A on changes in pathology, neutrophil infiltration, and pro-inflammatory cytokine levels in the mammary gland stimulated by lipopolysaccharide (LPS). Further, the effects of IL-17A on the activation of the nuclear factor-κB (NF-κB) signaling pathway during mastitis induced by LPS were also studied. The results showed that the production of IL-17A was significantly elevated during mastitis induced by LPS. IL-17A blockade via an intraperitoneal antibody injection protected against LPS-induced mastitis, as indicated by decreased neutrophil infiltration, myeloperoxidase activity, pro-inflammatory cytokines levels, and NF-κB signaling pathway molecule phosphorylation in response to LPS. In conclusion, an elevated IL-17 level plays a crucial role during mastitis, and anti-IL-17A antibody blockade protects against LPS-induced mammary gland inflammation induced through the NF-κB signaling pathway, which provides a new potential treatment target for mastitis. [ABSTRACT FROM AUTHOR]