Lipopolysaccharide (LPS) and lipoteichoic acid (LTA) are cell wall components of Escherichia coli and Staphylococcus aureus, which cause clinical and subclinical mastitis, respectively. However, the reason of the difference in symptoms by pathogen type remains unclear. In this study, the influence of LPS and LTA on early response and milk production in lactating bovine mammary epithelial cells (BMECs) was comparatively investigated. The results showed that LPS decreased the secretion of β-casein, lactose, and triglycerides, whereas LTA decreased the secretion of lactose and triglycerides but increased lactoferrin production without any influence on β-casein secretion. In addition, the influence of milk lipid droplet size in BMECs and gene expression related to milk fat synthesis was different between LPS and LTA. LPS increased the gene expression of interleukin (IL)-1β, tumor necrosis factor-α, and IL-8 through the activation of the nuclear factor-κB (NF-κB), p38, and c-Jun N-terminal kinase pathways, whereas LTA increased IL-1β and CC chemokine ligand 5 expression through the activation of the NF-κB pathway. Moreover, these cytokines and chemokines differently affected the milk production ability of BMECs. These results suggested that the pathogen-specific symptoms may be related to the differences in the early response of BMECs to bacterial toxins.

脂多糖 (LPS) 和脂磷壁酸 (LTA) 是大肠杆菌和金黄色葡萄球菌的细胞壁成分，分别引起临床和亚临床乳腺炎。然而，病原体类型导致症状差异的原因尚不清楚。本研究比较了 LPS 和 LTA 对泌乳牛乳腺上皮细胞 (BMECs) 早期反应和产奶量的影响。结果表明，LPS 减少了 β-酪蛋白、乳糖和甘油三酯的分泌，而 LTA 减少了乳糖和甘油三酯的分泌，但增加了乳铁蛋白的产生，而对 β-酪蛋白的分泌没有任何影响。此外，LPS和LTA对BMECs中乳脂滴大小和乳脂合成相关基因表达的影响不同。LPS 通过激活核因子-κB (NF-κB)、p38、和 c-Jun N 端激酶通路，而 LTA 通过激活 NF-κB 通路增加 IL-1β 和 CC 趋化因子配体 5 的表达。此外，这些细胞因子和趋化因子对 BMECs 的产奶能力有不同的影响。这些结果表明，病原体特异性症状可能与 BMECs 对细菌毒素早期反应的差异有关。