亲炎性CD14高CD16低单细胞/巨细胞在Treponema phagedenis-相关的牛数字皮肤炎中占主导地位
Priyoshi Lahiri1, Rakel Arrazuria1, Yi Lin Tan1
1Faculty of Veterinary Medicine, University of Calgary, Calgary, Canada.
Infection and immunity
|January 8, 2024
概括
牛的数字皮肤炎涉及由Treponema细菌引起的痛苦的脚病变. 这些病变中的亲炎性免疫细胞可能会阻止愈合,即使在数字皮肤炎的抗生素治疗后也是如此.
科学领域:
- 兽医皮肤病学 兽医皮肤病学
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
背景情况:
- 数字性皮肤炎 (DD) 是一种严重的牛足病,导致疼痛,性病变.
- DD与Treponema物种有关,但尽管治疗,但炎症的持续性尚不清楚.
- 了解DD的免疫反应对于开发有效治疗方法至关重要.
研究的目的:
- 为了研究活跃的数字性皮肤炎病变中的免疫细胞透.
- 探索Treponema phagedenis在诱导炎症反应中的作用.
- 阐明DD中巨细胞驱动的炎症机制.
主要方法:
- 在牛DD病变中分析免疫细胞群 (单细胞/巨细胞,中性粒细胞).
- 在小鼠中试验诱导,使用分离的Treponema phagedenis.
- 评估牛巨对T. phagedenis的反应,包括NLRP3炎症酶激活和IL-1β分泌.
主要成果:
- 活跃的DD病变显示出大量的亲炎性单细胞/巨细胞透,不受氧化环素治疗的影响.
- 在小鼠中注射T. phagedenis导致持久,其中有中性细胞和炎症性单细胞/巨细胞的招募.
- 用T. phagedenis刺激的牛巨细胞通过NLRP3炎症酶途径分泌IL-1β.
结论:
- 亲炎性单细胞/巨细胞和中性粒细胞是不愈合的DD病变的特征.
- 这些细胞主导的免疫反应可能会阻碍抗生素治疗后的伤口愈合.
- 准NLRP3炎症酶通路可能为数字性皮肤炎提供新的治疗策略.
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