Nrf2 and NF-?B/NLRP3 inflammasome pathways are involved in Prototheca bovis infections of mouse mammary gland tissue and mammary epithelial cells

Prototheca bovis is a serious pathogen for animals, but pathogenesis of P. bovis mastitis is unclear. The objective was to characterize how P. bovis induces inflammatory responses in mouse mammary gland tissue and mammary epithelial cells (mMECs). Prototheca bovis damaged mammary gland tissue and mitochondrial structure, and induced oxidative stress, as evident by significant increases in mtROS and MDA concentrations and significant decreases in T-SOD activity in both mammary gland tissue and mMECs. Expression of Nrf2, HO-1 and Keap1 proteins was significantly changed in mammary gland tissue and mMECs after P. bovis infection. Additionally, cytokines (IL-1 beta, IL-6 and IL-18) and protein expressions in NF-kappa B and in the NLRP3 inflammasome pathway were significantly increased in mammary gland tissue and mMECs. In the P. bovis group, treatment with N-acetylL-cysteine (NAC) significantly decreased protein expression in NF-kappa B and the NLRP3 inflammasome pathway, as well as IL-1 beta, IL-6 and IL-18, whereas protein expression in the Nrf2 pathway was significantly changed. Inhibition of NF-kappa B or NLRP3 significantly decreased expression of IL-1 beta and IL-18 proteins in mMECs infected with P. bovis. Additionally, activating Nrf2 inhibited expression of NLRP3 and IL-1 beta. In conclusion, P. bovis induced an inflammatory response via the NF-kappa B/NLRP3 inflammasome pathway; however, scavenging ROS or activating Nrf2 mitigated the inflammatory response in infected mMECs.

Automated summary

Prototheca bovis infection induces inflammatory responses in mouse mammary gland tissue and mammary epithelial cells. The NF-kappa B/NLRP3 inflammasome pathway plays a crucial role in the inflammatory response, while scavenging ROS or activating Nrf2 can mitigate this response.