Proteomic analysis of human immunodeficiency virus and periodontitis
Proteomic analysis of human immunodeficiency virus and periodontitis
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人类免疫缺陷病毒与牙周炎的蛋白质组学分析
DOI:
10.1080/14789450.2020.1879648
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发表时间:
2020
影响因子:
3.4
通讯作者:
Nakayama Tomohiro
中科院分区:
文献类型:
--
作者:
Tsuchida Sachio;Nakayama Tomohiro
Periodontal disease is a chronic oral infection that results from prolonged and persistent irritation of the supragingival tissue by dental biofilm buildup and can result in the destruction of connective tissue, cementum, the periodontal ligament, and the alveolar bone [1–3]. The findings of several studies have indicated a relationship between periodontitis and systemic and major lifestyle-related diseases, inasmuch as periodontitis is considered to be triggered by certain types of bacteria, poor dietary habits, and smoking [4–7]. Ahmad et al. reported that the majority of topics covered by the top 100 most widely read publications concerned the associations of periodontal disease with cardiovascular diseases (8598 citations) and with diabetes mellitus (7660 citations), followed by the systemic complications of periodontitis (mixed manifestations; 3918 citations), pregnancyrelated manifestations (10,909 citations), rheumatic manifestations (1955 citations), pulmonary manifestations (399 citations), cerebrovascular diseases (478 citations), and cancer (169 citations)[8]. However, the mechanisms underlying periodontitis are unclear. Bacterial pathogens are associated with the onset and progression of periodontal disease [9, 10]. Consideration of some of the more general aspects of microbial dental biofilm, including the development, heterogeneity, microbial succession, composition, structure, and mechanisms of dental biofilm formation, should precede the discussion of the microbial composition of the gingival crevice (subgingival dental biofilm). Dental biofilm is a collection of heterogeneous, dense, and non-calcified bacterial masses intimately associated with the tooth surface, and their firm adherence to the surface is usually considered to prevent their dislodgement with the salivary flow. Subgingival biofilms are nonadherent and comprise a large number of motile organisms. However, the detailed mechanism by which systemic disease is related to periodontal disease remains unclear. MS-based approaches can quantify enzyme levels in biological fluids, but they lack the capacity to measure their enzymatic activity [11]. The mechanistic aspects underlying the disease state are unknown, although the onset of periodontal disease is reportedly triggered by bacterial periodontal infection. Viruses may participate in the pathogenesis of periodontitis by altering immunological defenses or inducing destructive host reactions, or through direct lytic effects on periodontal tissue [12, 13]. Proteome, which defines the entire set of proteins that can be expressed by an organism, tissue, or cell, has attracted considerable attention because it can directly lead to the development of targeted therapeutics and identification of disease markers. In recent years, proteomic technology has been used to identify periodontitis biomarkers, with the discovery of several promising candidates as a result of exhaustive studies [14–17]. To determine the identity of biomarkers, extracted proteins are separated by one-and two-dimensional gel electrophoresis and their massto-charge ratios are measured with matrix-assisted laser desorption/ionization–time-of-flight (MALDI–TOF) mass spectrometry (MS). Liquid chromatography (LC)–MS, another tool used for protein identification, is particularly indispensable for screening proteins involved in inborn metabolism errors, toxicological analyses, and determining the efficacy of drugs. In addition, various immunoassays are frequently used to detect or measure steroid and peptide hormone concentrations. Historically, protein detection approaches have served as the basis to define a number of pathways regulated during the course of periodontal disease …
DOI:
10.1093/clinids/10.2.326
发表时间:
1988
期刊:
Reviews of infectious diseases
影响因子:
--
作者:
Abramson,JS;Mills,EL
通讯作者:
Mills,EL
影响因子:
3.4
作者:
Batschkus, Sarah;Cingoez, Goekhan;Lenz, Christof
通讯作者:
Lenz, Christof