Ren Meiyi, Jin Tianxiong, Tong Jingdi, Song Deyuan, Xie Qinna, Li Xiaohan, Li Yan, Liu Kangping, Gao Jian, Liu Mingchao, Cheng Jia
Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Hebei Agricultural University, Baoding 071001, China.
Key Laboratory of Healthy Breeding in Dairy Cattle (Co-Construction by Ministry and Province), Ministry of Agriculture and Rural Affairs, Hebei Agricultural University, Baoding 071001, China.
Animals (Basel). 2025 Apr 15;15(8):1139. doi: 10.3390/ani15081139.
Dairy cows are highly susceptible to mastitis caused by , and treating these infections poses a challenge due to the resistance of the bacterium to common antibiotics. This study aimed to evaluate the safety of SDS2.1 and investigate its protective effects against -induced mastitis. The safety of SDS2.1 was assessed through comprehensive analyses, including antibiotic resistance profiling, hemolysis assays, cell cytotoxicity tests, and whole-genome sequencing. Furthermore, its ability to protect against cellular and tissue damage caused by -induced mastitis was evaluated using both in vitro and in vivo models. Our results revealed that SDS2.1 was non-hemolytic, non-cytotoxic, and significantly inhibited the growth of ( < 0.05). Additionally, SDS2.1 effectively reduced the adhesion and invasion of . In the -induced mouse mastitis model, SDS2.1 significantly reduced myeloperoxidase (MPO) activity, mammary tissue damage, and the expression of inflammatory cytokines (IL-6, IL-1β, and TNF-α) ( < 0.05). In -infected bovine mammary epithelial cells (bMECs), SDS2.1 significantly decreased lactate dehydrogenase (LDH) release, indicating reduced cellular damage. These findings demonstrate that SDS2.1 exhibits anti-inflammatory properties in experimental models, suggesting its potential role in mitigating -induced mastitis.
奶牛极易感染由[细菌名称未给出]引起的乳腺炎，由于该细菌对常用抗生素具有抗性，治疗这些感染面临挑战。本研究旨在评估SDS2.1的安全性，并研究其对[细菌名称未给出]诱导的乳腺炎的保护作用。通过全面分析评估SDS2.1的安全性，包括抗生素抗性分析、溶血试验、细胞毒性测试和全基因组测序。此外，使用体外和体内模型评估其预防[细菌名称未给出]诱导的细胞和组织损伤的能力。我们的结果显示，SDS2.1无溶血作用、无细胞毒性，并显著抑制[细菌名称未给出]的生长（P<0.05）。此外，SDS2.1有效降低了[细菌名称未给出]的黏附和侵袭。在[细菌名称未给出]诱导的小鼠乳腺炎模型中，SDS2.1显著降低了髓过氧化物酶（MPO）活性、乳腺组织损伤以及炎性细胞因子（IL-6、IL-1β和TNF-α）的表达（P<0.05）。在[细菌名称未给出]感染的牛乳腺上皮细胞（bMECs）中，SDS2.1显著降低了乳酸脱氢酶（LDH）释放，表明细胞损伤减少。这些发现表明，SDS2.1在实验模型中表现出抗炎特性，提示其在减轻[细菌名称未给出]诱导的乳腺炎方面具有潜在作用。
