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The Role of Yersinia enterocolitica O:3 Lipopolysaccharide in Collagen-Induced Arthritis
Journal of Immunology Research ( IF 4.1 ) Pub Date : 2020-11-12 , DOI: 10.1155/2020/7439506
Katarzyna Kasperkiewicz 1 , Anna S Świerzko 2 , Marta Przybyła 3 , Janusz Szemraj 4 , Jarosław Barski 3 , Mikael Skurnik 5, 6 , Andrzej Kałużyński 7 , Maciej Cedzyński 2
Affiliation  

Yersinia enterocolitica O:3 is mentioned among the most common arthritogenic pathogens. Bacterial components (including lipopolysaccharide (LPS)) may persist in the joint after eradication of infection. Having an adjuvant activity, LPS may enhance production of anticollagen antibodies, involved in the pathogenesis of rheumatoid arthritis. Furthermore, its ability to activate complement contributes to the inflammation. The aim of this work was to investigate whether Yersinia LPS (coinjected with collagen) is associated with arthritis progression or other pathological effects and to elucidate the mechanism of this association. It was demonstrated that murine mannose-binding lectin C (MBL-C) recognizes the inner core heptoses of the Rd1 chemotype LPS of Yersinia. In addition, the Rd1 LPS activates the MBL-associated serine protease 1 (MASP-1) stronger than the S and Ra chemotype LPS and comparable to Klebsiella pneumoniae O:3 LPS. However, in contrast to the latter, Yersinia Rd1 LPS was associated neither with the adjuvancity nor with the enhancement of pathological changes in animal paws/impairment of motility. On the other hand, it seemed to be more hepatotoxic when compared with the other tested endotoxins, while the enlargement of inguinal lymph nodes and drop in hepatic MBL-C expression (at the mRNA level) were independent of LPS chemotype. Our data did not suggest no greater impact Y. enterocolitica O:3 on the development or severity of arthropathy related to anticollagen antibody-induced arthritis in mice, although its interaction with MBL-C and subsequent complement activation may contribute to some adverse effects.

中文翻译:

小肠结肠炎耶尔森菌 O:3 脂多糖在胶原诱导性关节炎中的作用

小肠结肠炎耶尔森氏菌O:3 是最常见的关节炎病原体之一。感染根除后,细菌成分(包括脂多糖 (LPS))可能会持续存在于关节中。LPS 具有佐剂活性,可增强抗胶原抗体的产生,参与类风湿性关节炎的发病机制。此外,它激活补体的能力有助于炎症。这项工作的目的是调查耶尔森氏菌LPS(与胶原蛋白共注射)是否与关节炎进展或其他病理效应有关,并阐明这种关联的机制。证明鼠甘露糖结合凝集素 C (MBL-C) 识别耶尔森氏菌Rd1 化学型 LPS 的内核庚糖此外,Rd1 LPS 激活 MBL 相关丝氨酸蛋白酶 1 (MASP-1) 比 S 和 Ra 化学型 LPS 更强,与肺炎克雷伯菌O:3 LPS相当。然而,与后者相反,耶尔森氏菌Rd1 LPS 既不与佐剂性相关,也不与动物爪子病理变化的增强/运动能力受损相关。另一方面,与其他测试的内毒素相比,它似乎更具肝毒性,而腹股沟淋巴结肿大和肝脏 MBL-C 表达(在 mRNA 水平)下降与 LPS 化学型无关。我们的数据并未表明Y没有更大的影响。小肠结肠炎 O:3 关于与小鼠抗胶原抗体诱导的关节炎相关的关节病的发展或严重程度,尽管它与 MBL-C 的相互作用和随后的补体激活可能会导致一些不良反应。
更新日期:2020-11-12
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