周周病原体通过表面附着蛋白酶从人类的氨酸-氨酸系统降解血管新素I
Irena Waligórska1, Krzysztof M Żak2, Natalia Mikrut3
1Department of Microbiology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Kraków, Poland. irena.waligorska@gmail.com.
Scientific reports
|November 28, 2025
概括
口腔病原体 Porphyromonas gingivalis 和 Tannerella forsythia 使用 PepO 蛋白酶调节 氨酸 - 血管新生素 系统 (RAS). 这些细菌引导RAS产生Ang 1-7,影响血压调节.
科学领域:
- 微生物学 微生物学
- 生物化学 生物化学
- 生理学 生理学 生理学
背景情况:
- 氨酸 - 血管素系统 (RAS) 通过血管素 (Ang) 调节血压.
- 口腔病原体 Porphyromonas gingivalis (Pg) 和 Tannerella forsythia (Tf) 都与系统性疾病有关.
- 口腔病原体与宿主系统 (如RAS) 相互作用的具体机制尚未完全理解.
研究的目的:
- 研究口腔病原体Pg和Tf在调节氨酸-血管新生素系统 (RAS) 中的作用.
- 为了确定负责血管素水解的特定细菌蛋白酶.
- 描述这些蛋白酶的酶性质和结构特征.
主要方法:
- 使用合成基质进行酶活性测定以表征PepO蛋白酶.
- 确定TfPepO的晶体结构,以阐明其催化机制.
- 免疫测试检测PepO在外膜囊泡中的释放.
- 盖勒里亚梅隆氏菌感染模型用于评估细菌毒性.
主要成果:
- Pg 和 Tf 具有 PgPepO 和 TfPepO 的内酶,它们能化 Angiotensin I (Ang I).
- 由于其广泛的催化裂,TfPepO具有独特的基质水解特性.
- 佩波蛋白酶通过外膜囊泡从细菌细胞表面释放出来.
- 在Galleria mellonella模型中,PepO删除显著降低了Tf的毒性.
结论:
- 来自Pg和Tf的PepO蛋白酶是Ang I的水解中的关键介质.
- 这些细菌蛋白酶可以通过指导血管素的产生来调节宁-血管素系统 (RAS).
- 这些发现揭示了口腔病原体与宿主生理系统之间相互作用的新机制.
相关概念视频
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
2.3K
Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
2.3K
Antihypertensive Drugs: Direct Renin Inhibitors
1.2K
The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
1.2K
Role of Matrix Metalloproteases in Degradation of ECM
3.2K
Matrix metalloproteases (MMPs) are enzymes involved in the hydrolysis of proteins and glycoproteins of the extracellular matrix. MMPs are essential for the migration and proliferation of cells through the dense matrix network, throughout embryonic development, and throughout morphogenesis. The first MMP activity discovered was a collagenase in a tadpole's tail undergoing metamorphosis. The active collagen deposition and modifications lead to the morphogenesis of tadpoles into the adult...
3.2K
Hypertension II: Pathophysiology
708
Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
708
Antihypertensive Drugs: Angiotensin II Receptor Blockers
2.4K
In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
2.4K
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
888
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
888


