Department of Surgery, School of Medicine, Complutense University of Madrid, 28040 Madrid, Spain.
Department of Physiology, School of Medicine, Autonomous University of Madrid, 28049 Madrid, Spain.
Cells. 2019 Jun 29;8(7):658. doi: 10.3390/cells8070658.
Portal hypertension is a common complication of liver disease, either acute or chronic. Consequently, in chronic liver disease, such as the hypertensive mesenteric venous pathology, the coexisting inflammatory response is classically characterized by the splanchnic blood circulation. However, a vascular lymphatic pathology is produced simultaneously with the splanchnic arterio-venous impairments. The pathological increase of the mesenteric venous pressure, by mechanotransduction of the venous endothelium hyperpressure, causes an inflammatory response involving the subendothelial mast cells and the lymphatic endothelium of the intestinal villi lacteal. In portal hypertension, the intestinal lymphatic inflammatory response through the development of mesenteric-systemic lymphatic collateral vessels favors the systemic diffusion of substances with a molecular pattern associated with damage and pathogens of intestinal origin. When the chronic hepatic insufficiency worsens the portal hypertensive inflammatory response, the splanchnic lymphatic system transports the hyperplasied intestinal mast cells to the mesenteric lymphatic complex. Then, an acquired immune response regulating a new hepato-intestinal metabolic scenario is activated. Therefore, reduction of the hepatic metabolism would reduce its key centralized functions, such as the metabolic, detoxifying and antioxidant functions which would try to be substituted by their peroxisome activity, among other functions of the mast cells.
门静脉高压症是肝脏疾病的常见并发症,无论是急性还是慢性的。因此,在慢性肝病中,如高血压性肠系膜静脉病理学,共存的炎症反应通常以内脏血液循环为特征。然而,同时也会产生血管淋巴管病理学。肠系膜静脉压力病理性升高,通过静脉内皮高压的机械转导,导致涉及肠绒毛乳糜管的黏膜下肥大细胞和淋巴管内皮的炎症反应。在门静脉高压症中,通过肠系膜-系统淋巴侧支血管的发展,肠道淋巴炎症反应有利于与肠道来源的损伤和病原体相关的具有分子模式的物质向全身扩散。当慢性肝功能不全使门静脉高压炎症反应恶化时,内脏淋巴系统将过度增生的肠道肥大细胞运送到肠系膜淋巴复合体。然后,激活调节新的肝肠代谢情景的获得性免疫反应。因此,减少肝脏代谢会降低其关键集中功能,如代谢、解毒和抗氧化功能,这些功能将试图通过其过氧化物酶体活性以及肥大细胞的其他功能来替代。