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PPD和hsp65诱导的单关节炎引发Lewis大鼠自发性复发性发作。

PPD and hsp65 induced monoarthritis initiates spontaneous recurrent flares in Lewis rats.

作者信息

Ragno S, Morris C J, Coumbe A, Mapp P I, Colston M J, Blake D R, Winrow V R

机构信息

ARC Bone and Joint Research Unit, London Hospital Medical College, United Kingdom.

出版信息

Ann Rheum Dis. 1995 Jan;54(1):59-65. doi: 10.1136/ard.54.1.59.

DOI:10.1136/ard.54.1.59
PMID:7880124
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1005514/
Abstract

OBJECTIVES

To investigate the time course of a monoarthritis induced with the purified protein derivative of tuberculin (PPD) or a recombinant 65 kDa heat shock protein (rhsp65) in two different strains of sensitised rats.

METHODS

Wistar and Lewis rats, sensitised with heat killed Mycobacterium tuberculosis in oil, were challenged intraarticularly with PPD or rhsp65 and monitored for six weeks. Inflammation was assessed by joint swelling, histology, and radiographic studies.

RESULTS

Sensitised Lewis rats injected with PPD or rhsp65 showed a chronic response with recurrent spontaneous flares, while Wistar rats showed one inflammatory episode.

CONCLUSIONS

The Wistar strain response to PPD resembles a transient reactive arthritis, while the response of the Lewis strain mimics the relapsing nature of rheumatoid synovitis, providing an interesting model to determine dominant immunopathogenic mechanisms.

摘要

目的

研究在两种不同品系的致敏大鼠中，用结核菌素纯蛋白衍生物（PPD）或重组65 kDa热休克蛋白（rhsp65）诱导单关节炎的时间进程。

方法

用热灭活的结核分枝杆菌油剂致敏的Wistar和Lewis大鼠，通过关节内注射PPD或rhsp65进行攻击，并监测六周。通过关节肿胀、组织学和放射学研究评估炎症。

结果

注射PPD或rhsp65的致敏Lewis大鼠表现出慢性反应，伴有反复的自发发作，而Wistar大鼠表现出一次炎症发作。

结论

Wistar品系对PPD的反应类似于短暂性反应性关节炎，而Lewis品系的反应模仿类风湿性滑膜炎的复发性质，为确定主要的免疫致病机制提供了一个有趣的模型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2f3/1005514/4afc8889e904/annrheumd00501-0072-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2f3/1005514/d4c3929cf66b/annrheumd00501-0071-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2f3/1005514/4afc8889e904/annrheumd00501-0072-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2f3/1005514/d4c3929cf66b/annrheumd00501-0071-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2f3/1005514/4afc8889e904/annrheumd00501-0072-a.jpg

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本文引用的文献

1
A reappraisal of the evidence that rheumatoid arthritis and several other idiopathic diseases are slow bacterial infections.对类风湿性关节炎和其他几种特发性疾病是慢性细菌感染这一证据的重新评估。
Ann Rheum Dis. 1993 Mar;52 Suppl 1(Suppl 1):S30-8. doi: 10.1136/ard.52.suppl_1.s30.
2
Rheumatoid arthritis: how well do the theories fit the evidence?类风湿性关节炎：这些理论与证据的契合程度如何？
Clin Exp Immunol. 1993 Apr;92(1):1-6. doi: 10.1111/j.1365-2249.1993.tb05938.x.
3
T cells are responsible for the enhanced synovial cellular immune response to triggering antigen in reactive arthritis.
T细胞在反应性关节炎中负责增强滑膜对触发抗原的细胞免疫反应。
Clin Exp Immunol. 1993 Jan;91(1):96-102. doi: 10.1111/j.1365-2249.1993.tb03361.x.
4
Bacterial cell wall polymers (peptidoglycan-polysaccharide) cause reactivation of arthritis.细菌细胞壁聚合物（肽聚糖 - 多糖）会引发关节炎复发。
Infect Immun. 1993 Nov;61(11):4645-53. doi: 10.1128/iai.61.11.4645-4653.1993.
5
Can immunisation trigger rheumatoid arthritis?免疫接种会引发类风湿性关节炎吗？
Ann Rheum Dis. 1993 Dec;52(12):843-4. doi: 10.1136/ard.52.12.843.
6
Arthritogenic potential of the 65 kDa stress protein--an experimental model.65 kDa应激蛋白的致关节炎潜力——一种实验模型
Ann Rheum Dis. 1994 Mar;53(3):197-201. doi: 10.1136/ard.53.3.197.
7
Priming to heat shock proteins in infants vaccinated against pertussis.百日咳疫苗接种婴儿对热休克蛋白的致敏作用。
J Immunol. 1993 Mar 1;150(5):2025-32.
8
Inflammation activates self hsp60-specific T cells.炎症激活自身热休克蛋白60特异性T细胞。
Eur J Immunol. 1993 Jan;23(1):33-8. doi: 10.1002/eji.1830230107.
9
Sequential alterations of periarticular structures in antigen-induced arthritis in mice. Histological observations on fibrous capsule, ligaments, bone and muscles, using whole joint sections.小鼠抗原诱导性关节炎中关节周围结构的序贯改变。使用全关节切片对纤维囊、韧带、骨骼和肌肉进行组织学观察。
Br J Exp Pathol. 1983 Jun;64(3):298-305.
10
Exacerbation of antigen-induced arthritis after challenge with intravenous antigen.静脉注射抗原激发后抗原诱导性关节炎的加重
Immunology. 1983 May;49(1):161-7.