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细菌和宿主酶调节由莱姆病病原体的酸甘产生的炎症反应

Joshua W McCausland^1,2,3, Zachary A Kloos⁴, Irnov Irnov^1,3

¹Sarafan ChEM-H Institute, Stanford University, Stanford, CA, USA.

bioRxiv : the preprint server for biology

|January 20, 2025

概括

博雷利亚堡多弗里 (Borrelia burgdorferi peptidoglycan) (PG^Bb) 碎片有助于莱姆病关节炎的发生. 细菌酶MltS修改PG^Bb,减少免疫检测,而宿主酶PGLYRP2在关节中的活性较低,可能增加炎症.

科学领域:

微生物学和免疫学
细菌病原体的产生
宿主-病原体相互作用

背景情况:

博雷利亚菌 (Borrelia burgdorferi) 引起莱姆病,关节持续炎症可能导致关节炎.
抗原B. burgdorferi丁糖 (PG^Bb) 碎片可能会在关节中持续存在,即使在抗生素治疗后也会导致免疫病理.
与其他细菌不同,B. burgdorferi由于缺乏回收活动而释放PG^Bb循环产品.

研究的目的:

为了识别从B. burgdorferi释放的PG^Bb片段.
研究细菌酶在PG^Bb修饰和免疫逃避中的作用.
了解宿主免疫因子在关节组织中对莱姆病关节炎发病的贡献.

主要方法:

质谱法被用来识别释放的PG^Bb片段.
生物化学试验描述了B. burgdorferi蛋白质BB0605 (DacA) 和BB0259 (MltS) 的酶活性.
用合成PG^Bb片段刺激人类细胞系,并测量免疫反应. 评估了PGLYRP2在突液和血清中的活性.

主要成果:

B. burgdorferi释放PG^Bb片段,转换发生在合成部位 (DacA活性) 和溶性转糖酶活性 (MltS) 产生1,6-无水PG^Bb片段.
与水合碎片相比,1,6-无水PG^Bb碎片是NOD2依赖性免疫反应的较差诱导剂.
人类突液的PGLYRP2活性低于血清,这表明减少减少关节PG^Bb免疫性的能力.

结论:

MltS活动有助于B. burgdorferi通过修改棚PG^Bb片段来逃避NOD2介导的免疫检测.
莱姆病中PG^Bb诱导的免疫病理可能源于宿主对溶解螺旋体碎片的识别.
主体PGLYRP2活性的变化可能会影响不同组织和个体对PG诱导炎症的易感性.

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