Zhang Bohao, Chen Na, Yu Xing, Li Jianfu, Dong Weitao, Zhang Yong, Zhao Xingxu, Zhang Quanwei
College of Veterinary Medicine, Gansu Agriculture University, Lanzhou 730070, China.
College of Life Science and Technology, Gansu Agriculture University, Lanzhou 730070, China.
Biomolecules. 2025 Jun 6;15(6):827. doi: 10.3390/biom15060827.
Immune homeostasis refers to the immune system's ability to maintain a dynamic balance, defend against infections while preventing excessive inflammation, and preserve normal physiological activity. However, its regulatory role in the mammary glands (MGs) of cows with clinical mastitis (CM) remains unclear. This study examined MG tissue samples collected from healthy Holstein cows and those with CM caused by ( = three per group) to identify candidate biomolecular targets involved in immune homeostasis in dairy cows affected by mastitis through a proteomics-based bioinformatic analysis and analyze their expression and localization in MG tissues. A pathological examination revealed that the MG tissues of the CM group exhibited significant alveoli collapse and inflammatory cell infiltration. The presence of activated phagolysosomes and lysosomes indicated active immune and phagocytic responses. Bioinformatics highlighted coronin1A (CORO1A) as a potential modulator of immune responses through phagosome formation. Dysregulation could impair immune homeostasis, thereby exacerbating mastitis. Immunofluorescence and immunohistochemistry staining showed that CORO1A was localized in monocytes, macrophages, and neutrophils. Molecular mechanism analysis revealed that Toll-like receptor 2 (TLR2) recognizes pathogens and recruits CORO1A to the phagosome formation site, thereby enhancing the phagocytic activity of immune cells. The expression levels of and mRNA and proteins were positively correlated with the incidence of mastitis. In conclusion, CORO1A upregulation may activate immune and phagocytic responses, disrupting MGs' immune homeostasis during -induced mastitis. These findings provide novel insights into mastitis pathogenesis and potential therapeutic targets.
免疫稳态是指免疫系统维持动态平衡的能力，既能抵御感染又能防止过度炎症，并保持正常生理活动。然而，其在临床型乳房炎（CM）奶牛乳腺中的调节作用仍不清楚。本研究检查了从健康荷斯坦奶牛以及患有CM的奶牛（每组三头）采集的乳腺组织样本，通过基于蛋白质组学的生物信息学分析来鉴定参与乳腺炎影响的奶牛免疫稳态的候选生物分子靶点，并分析它们在乳腺组织中的表达和定位。病理检查显示，CM组的乳腺组织出现明显的肺泡塌陷和炎性细胞浸润。活化的吞噬溶酶体和溶酶体的存在表明存在活跃的免疫和吞噬反应。生物信息学强调冠蛋白1A（CORO1A）是通过吞噬体形成调节免疫反应的潜在调节因子。失调可能损害免疫稳态，从而加重乳腺炎。免疫荧光和免疫组织化学染色显示，CORO1A定位于单核细胞、巨噬细胞和中性粒细胞。分子机制分析表明，Toll样受体2（TLR2）识别病原体并将CORO1A募集到吞噬体形成位点，从而增强免疫细胞的吞噬活性。CORO1A的mRNA和蛋白质表达水平与乳腺炎发病率呈正相关。总之，CORO1A上调可能激活免疫和吞噬反应，在[病原体名称未给出]诱导的乳腺炎期间破坏乳腺的免疫稳态。这些发现为乳腺炎发病机制和潜在治疗靶点提供了新的见解。
