Biochemical and molecular characteristics of Porphyromonas gingivalis a key causative pathogen in periodontitis

IF 0.2 Q4 MEDICINE, GENERAL & INTERNAL
Shivani Sachdeva, H. Saluja, A. Mani
{"title":"Biochemical and molecular characteristics of Porphyromonas gingivalis a key causative pathogen in periodontitis","authors":"Shivani Sachdeva, H. Saluja, A. Mani","doi":"10.4103/jhnps.jhnps_92_22","DOIUrl":null,"url":null,"abstract":"Periodontitis is an infection-driven inflammatory disease, which is characterized by gingival inflammation and bone loss. Periodontitis is associated with various systemic diseases, including cardiovascular, respiratory, musculoskeletal, and reproductive system-related abnormalities. The recent theory attributes the pathogenesis of periodontitis to oral microbial dysbiosis, in which Porphyromonas gingivalis acts as a critical agent by disrupting host immune homeostasis. Lipopolysaccharide, proteases, fimbriae, and some other virulence factors are among the strategies exploited by P. gingivalis to promote the bacterial colonization and facilitate the outgrowth of the surrounding microbial community. Virulence factors promote the coaggregation of P. gingivalis with other bacteria and the formation of dental biofilm. These virulence factors also modulate a variety of host immune components and subvert the immune response to evade bacterial clearance or induce an inflammatory environment. The antibody-based concept of P. gingivalis as a causative agent in human periodontitis is based on the humoral immune response; P. gingivalis is probably a causative agent in periodontal disease, and this humoral immune response is probably protective. P. gingivalis fimbriae promote monocytes and macrophage activation. Stimulation of memory T-cells derived from periodontitis patient with P. gingivalis has been shown to induce higher interleukin (IL)-4 production than in healthy controls. The induction of IL-4-producing memory T-cells in peripheral blood tended to coincide with that of autologous periodontitis lesion sites. The article focuses to discuss the virulence factors of periodontal pathogens, especially P. gingivalis, and their roles in regulating immune responses during periodontitis progression.","PeriodicalId":41774,"journal":{"name":"Journal of Head & Neck Physicians and Surgeons","volume":null,"pages":null},"PeriodicalIF":0.2000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Head & Neck Physicians and Surgeons","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4103/jhnps.jhnps_92_22","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
引用次数: 0

Abstract

Periodontitis is an infection-driven inflammatory disease, which is characterized by gingival inflammation and bone loss. Periodontitis is associated with various systemic diseases, including cardiovascular, respiratory, musculoskeletal, and reproductive system-related abnormalities. The recent theory attributes the pathogenesis of periodontitis to oral microbial dysbiosis, in which Porphyromonas gingivalis acts as a critical agent by disrupting host immune homeostasis. Lipopolysaccharide, proteases, fimbriae, and some other virulence factors are among the strategies exploited by P. gingivalis to promote the bacterial colonization and facilitate the outgrowth of the surrounding microbial community. Virulence factors promote the coaggregation of P. gingivalis with other bacteria and the formation of dental biofilm. These virulence factors also modulate a variety of host immune components and subvert the immune response to evade bacterial clearance or induce an inflammatory environment. The antibody-based concept of P. gingivalis as a causative agent in human periodontitis is based on the humoral immune response; P. gingivalis is probably a causative agent in periodontal disease, and this humoral immune response is probably protective. P. gingivalis fimbriae promote monocytes and macrophage activation. Stimulation of memory T-cells derived from periodontitis patient with P. gingivalis has been shown to induce higher interleukin (IL)-4 production than in healthy controls. The induction of IL-4-producing memory T-cells in peripheral blood tended to coincide with that of autologous periodontitis lesion sites. The article focuses to discuss the virulence factors of periodontal pathogens, especially P. gingivalis, and their roles in regulating immune responses during periodontitis progression.
牙周炎主要病原菌牙龈卟啉单胞菌的生化和分子特征
牙周炎是一种感染驱动的炎症性疾病,其特征是牙龈炎症和骨质流失。牙周炎与多种全身性疾病有关,包括心血管、呼吸、肌肉骨骼和生殖系统相关异常。最近的理论将牙周炎的发病机制归因于口腔微生物生态失调,其中牙龈卟啉单胞菌通过破坏宿主免疫稳态而发挥关键作用。脂多糖、蛋白酶、菌毛和其他一些毒力因子是牙龈卟啉卟啉菌促进细菌定植和促进周围微生物群落生长的策略。毒力因子促进牙龈假单胞菌与其他细菌共聚集,形成牙生物膜。这些毒力因子还调节多种宿主免疫成分,破坏免疫反应以逃避细菌清除或诱导炎症环境。基于抗体的牙龈假单胞菌作为人类牙周炎病原体的概念是基于体液免疫反应;牙龈卟啉卟啉菌可能是牙周病的病原体,而这种体液免疫反应可能具有保护作用。牙龈卟啉菌毛促进单核细胞和巨噬细胞的活化。刺激牙龈假单胞菌牙周炎患者的记忆t细胞可诱导比健康对照组更高的白细胞介素(IL)-4的产生。外周血中产生il -4记忆t细胞的诱导倾向于与自体牙周炎病变部位一致。本文就牙周病原菌的毒力因子,特别是牙龈假单胞菌的毒力因子及其在牙周炎发展过程中调节免疫应答的作用作一综述。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Journal of Head & Neck Physicians and Surgeons
Journal of Head & Neck Physicians and Surgeons MEDICINE, GENERAL & INTERNAL-
CiteScore
0.30
自引率
0.00%
发文量
0
审稿时长
15 weeks
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信