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牛奶细胞对导致乳腺炎的Streptococcus uberis持续性和短暂性菌株的不同细胞和分子反应

Anyaphat Srithanasuwan^1,2, Ynte H Schukken^2,3,4, Noppason Pangprasit^1,5

¹Faculty of Veterinary Medicine, Chiang Mai University, Chiang Mai, Thailand.

|January 11, 2024

概括

过渡性Streptococcus uberis菌株在奶牛中引发更强的免疫反应,导致乳腺炎更快地恢复. 持久菌株诱导不同的炎症途径,这表明囊形成会影响免疫逃避.

科学领域:

兽医免疫学兽医免疫学
细菌学细菌学是一门学科.
乳制品科学乳制品科学

背景情况:

杆菌 (Streptococcus uberis) 在奶牛中引起乳腺炎,感染的持续时间和严重程度各不相同.
细菌的毒性和宿主免疫力决定了感染的结果,从亚临床炎症到严重的短暂性乳腺炎.

研究的目的:

为了比较牛奶分离的白细胞 (mWBC) 与持久和短暂的S. uberis菌株的炎症反应.
探究导致对S. uberis. 不同免疫反应的分子机制.

主要方法:

在10周内每周收集四分之一的牛奶样本进行细菌培养.
根据感染持续时间和PFGE.选择过渡性 (非囊) 和持久性 (囊) S. uberis菌株.
评估了mWBCs的细胞反应 (迁移,ROS生成,杀死细菌,NET释放) 和分子反应 (TLRs和TNF-α的基因表达).

主要成果:

过渡性S. uberis在迁移,反应性氧物种生成和杀死细菌方面引起了更强的mWBC反应.
持续的S. uberis诱导了中性粒细胞细胞外陷 (NET) 释放的增加.
过渡性菌株显著上调了mWBCs中的TLR-1,TLR-2,TLR-6和TNF-α基因表达.

结论:

过渡性S. uberis菌株在奶牛中诱导更强大的局部免疫反应,促进更快的乳腺炎解决.
在S. uberis中形成囊可能在免疫逃避和持久感染中起作用.
了解这些差异性免疫反应可以为乳腺炎管理策略提供信息.

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