Wang Heng, Yu Guangtao, Yu Hui, Gu Mingjie, Zhang Jun, Meng Xia, Liu Zongping, Qiu Changwei, Li Jianji
College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, 225009, China.
Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, Jiangsu, 225009, China.
Acta Vet Scand. 2015 May 20;57:25. doi: 10.1186/s13028-015-0116-0.
Staphylococcus aureus causes subclinical mastitis as well as persistent and chronic infections in cattle. Bovine mastitis induced by S. aureus is often refractory to antibiotic treatment. Local innate immune defenses play an important role in eliminating the invading bacteria. TLR2 and NOD2 are important pathogen recognition receptors, but their functions have not been investigated in the context of early stages of mastitis. The present study examined TLR2, NOD2, and related cytokines in mammary glands infection induced by S. aureus at early stages in a rat mastitis model.
All inoculated mammary glands developed mastitis. Acute changes were induced in mammary tissues infected with S. aureus at early stages and then chronic infections persisted until the end of the experiment. TLR2 and NOD2 mRNA expression increased significantly after inoculation with S. aureus. The expression levels of cytokine mRNAs, including TNF-α, IL-1β, IL-6, IL-10, and CXCL1, also increased. TGF-β1 expression was suppressed at early phase and IFN-γ mRNA expression increased significantly at a later stage.
Mammary innate immune responses were activated after S. aureus inoculation. TLR2, NOD2, and inflammatory cytokines (TNF-α, IL-1β, IL-6, CXCL1, IL-10, TGF-β1, and IFN-γ) are involved in the response to mastitis induced by S. aureus.
金黄色葡萄球菌可引起奶牛亚临床乳腺炎以及持续性和慢性感染。由金黄色葡萄球菌引起的牛乳腺炎通常对抗生素治疗具有抗性。局部先天免疫防御在清除入侵细菌方面发挥着重要作用。Toll样受体2(TLR2)和核苷酸结合寡聚化结构域蛋白2(NOD2)是重要的病原体识别受体,但它们在乳腺炎早期阶段的功能尚未得到研究。本研究在大鼠乳腺炎模型中检测了金黄色葡萄球菌诱导的乳腺感染早期阶段的TLR2、NOD2及相关细胞因子。
所有接种的乳腺均发生了乳腺炎。早期感染金黄色葡萄球菌的乳腺组织出现急性变化,随后慢性感染持续至实验结束。接种金黄色葡萄球菌后,TLR2和NOD2 mRNA表达显著增加。包括肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、白细胞介素-10(IL-10)和CXC趋化因子配体1(CXCL1)在内的细胞因子mRNA表达水平也升高。转化生长因子-β1(TGF-β1)表达在早期受到抑制,干扰素-γ(IFN-γ)mRNA表达在后期显著增加。
接种金黄色葡萄球菌后乳腺先天免疫反应被激活。TLR2、NOD2和炎性细胞因子(TNF-α、IL-1β、IL-6、CXCL1、IL-10、TGF-β1和IFN-γ)参与了对金黄色葡萄球菌诱导的乳腺炎的反应。