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疑似主要牙周病原体对免疫球蛋白A2、A2和G的降解作用。

Degradation of immunoglobulins A2, A2, and G by suspected principal periodontal pathogens.

作者信息

Kilian M

出版信息

Infect Immun. 1981 Dec;34(3):757-65. doi: 10.1128/iai.34.3.757-765.1981.

DOI:10.1128/iai.34.3.757-765.1981
PMID:7037640
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC350936/
Abstract

Attention has recently been focused on immunoglobulin A1 (IgA1) protease production as a possible virulence factor of bacteria implicated in meningitis and gonorrhea. This report demonstrates that suspected principal etiological agents in destructive periodontal disease include bacteria capable of degrading IgA1, IgA2, and IgG. Representative strains of Bacteroides melaninogenicus subsp. melaninogenicus and Capnocytophaga cleaved IgA1 but not IgA2 in the hinge region to yield intact Fab and Fc fragments. All Capnocytophaga strains also cleaved IgG in the same way. The majority of strains of Bacteroides asaccharolyticus and B. melaninogenicus subsp. intermedius caused complete degradation of both IgA1 and polyclonal IgG. However, some strains left the Fc part of IgA1 intact. Several strains were also capable of completely decomposing IgA2 and S-IgA. Significant IgA-cleaving enzyme activity was detected in whole subgingival dental plaque collected from patients with destructive periodontal disease. The results indicate that colonization of the subgingival area by B. asaccharolyticus, B. melaninogenicus, and Capnocytophaga spp. can induce a local paralysis of the immune defence mechanisms, thereby facilitating the penetration and spread of potentially toxic substances, lytic enzymes, and antigens released by the entire subgingival microflora.

摘要

最近,免疫球蛋白A1(IgA1)蛋白酶的产生作为与脑膜炎和淋病相关细菌的一种可能毒力因子受到了关注。本报告表明,破坏性牙周病中疑似主要病原体包括能够降解IgA1、IgA2和IgG的细菌。产黑色素拟杆菌黑色素亚种和二氧化碳嗜纤维菌的代表性菌株在铰链区切割IgA1而不切割IgA2,产生完整的Fab和Fc片段。所有二氧化碳嗜纤维菌菌株也以同样的方式切割IgG。大多数解糖拟杆菌和产黑色素拟杆菌中间亚种菌株导致IgA1和多克隆IgG完全降解。然而,一些菌株使IgA1的Fc部分保持完整。一些菌株还能够完全分解IgA2和分泌型IgA。在从患有破坏性牙周病的患者收集的全龈下牙菌斑中检测到显著的IgA切割酶活性。结果表明,解糖拟杆菌、产黑色素拟杆菌和二氧化碳嗜纤维菌属在龈下区域的定植可诱导免疫防御机制的局部麻痹,从而促进整个龈下微生物群释放的潜在有毒物质、裂解酶和抗原的渗透和扩散。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0b6/350936/0fb779451ae8/iai00158-0134-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0b6/350936/8c7f52a6b37b/iai00158-0132-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0b6/350936/b85960717ea9/iai00158-0132-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0b6/350936/a2cd72c18aca/iai00158-0133-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0b6/350936/d876371f527e/iai00158-0133-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0b6/350936/0fb779451ae8/iai00158-0134-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0b6/350936/8c7f52a6b37b/iai00158-0132-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0b6/350936/b85960717ea9/iai00158-0132-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0b6/350936/a2cd72c18aca/iai00158-0133-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0b6/350936/d876371f527e/iai00158-0133-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0b6/350936/0fb779451ae8/iai00158-0134-a.jpg

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