探索肠道血管屏障蛋白在艾滋病毒引起的粘膜损伤中的作用:一项比较研究
1Department of Dermatology, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
AIDS research and human retroviruses
|November 6, 2024
概括
艾滋病毒感染者 (PLWH) 肠道粘膜损伤增加和肠道血管屏障 (GVB) 发生变化. 血囊泡相关蛋白 (PLVAP) 表达表明PLWH中的GVB损伤和疾病进展.
科学领域:
- 胃肠病学 胃肠病学
- 免疫学 免疫学 免疫学
- 病毒学 病毒学
背景情况:
- 人类免疫缺陷病毒 (HIV) 感染与胃肠道并发症有关.
- 肠道血管屏障 (GVB) 的完整性对肠道健康至关重要.
- GVB蛋白质的改变可能会导致艾滋病毒感染者 (PLWH) 的肠道损伤.
研究的目的:
- 为了比较肠粘膜损伤和GVB蛋白表达 (occludin,ZO-1,VE-cadherin,β-catenin,PLVAP) 在PLWH,无症状PLWH和健康对照中.
- 调查GVB变化与PLWH疾病状况之间的关系.
- 为了确定HIV感染中GVB损伤的潜在生物标志物.
主要方法:
- 从PLWH,无症状PLWH和非PLWH (健康对照) 收集了结肠粘膜组织样本.
- 组织学检查 (血素和欧染色) 评估了粘膜损伤.
- 通过RT-qPCR,免疫组织化学和西部涂抹分析了GVB蛋白的表达 (occludin,ZO-1,VE-cadherin,β-catenin,PLVAP).
主要成果:
- 与非PLWH相比,PLWH和无症状PLWH的结肠粘膜损伤得分明显高.
- 与无症状的PLWH和非PLWH相比,PLWH中的PLVAP蛋白水平较高.
- 与非PLWH相比,PLWH的ZO-1表达显著较低,而与非PLWH相比,PLVAP表达在PLWH和无症状PLWH中较高.
- CD4+ T细胞计数和CD4+/CD8+ T细胞比率在各组之间有显著差异,与疾病状况相关.
结论:
- PLWH经历了显著的肠粘膜炎症和GVB损伤.
- 结肠粘膜中PLVAP表达升高与艾滋病毒感染有关,并可能作为GVB损伤和疾病进展的指标.
- 准GVB完整性可能是管理PLWH中胃肠道并发症的治疗策略.
更多相关视频
相关概念视频
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
356
Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI) tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
356
Mucosal Barrier of the Stomach
526
The gastric glands contain parietal cells that secrete hydrochloric acid (HCl) for digestion. The cells secrete HCl because it is highly corrosive and essential for breaking down food. To achieve this, they secrete hydrogen and chloride ions into the lumen of the gastric glands, which combine to form HCl.
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
526
Surface Membrane Barriers
1.1K
The skin and mucous membranes serve as the primary line of defense against pathogens by providing both physical and chemical protection. These barriers are essential in preventing the entry and establishment of microbes, thereby maintaining the integrity of the host.
The outer layer of the skin, the epidermis, is a robust barrier comprising layers of closely packed keratinized cells. This dense arrangement prevents microbes from penetrating the body. The periodic shedding of epidermal cells...
The outer layer of the skin, the epidermis, is a robust barrier comprising layers of closely packed keratinized cells. This dense arrangement prevents microbes from penetrating the body. The periodic shedding of epidermal cells...
1.1K
Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents
390
In the intricate landscape of the gastric lumen, excessive acid secretion disrupts the natural defense mechanisms, weakening the mucus-bicarbonate barrier. This vulnerability allows pepsin to infiltrate epithelial cells, digesting mucosal proteins and triggering erosion, leading to ulcer formation.
In this scenario, mucosal protective agents like sucralfate play an essential role. Sucralfate, a complex of sulfated sucrose and aluminum hydroxide, demonstrates its usefulness in acidic conditions,...
In this scenario, mucosal protective agents like sucralfate play an essential role. Sucralfate, a complex of sulfated sucrose and aluminum hydroxide, demonstrates its usefulness in acidic conditions,...
390
Peptic Ulcer Disease II: Pathophysiology
297
Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
297


