期刊
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
卷 320, 期 2, 页码 L266-L275出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00046.2020
关键词
acute lung injury; mast cells; orthotopic liver transplantation; polymorphonuclear neutrophils apoptosis
资金
- National Natural Science Foundation of China [81600507]
This study found that mast cell activation and polymorphonuclear neutrophil apoptosis were associated with acute lung injury after orthotopic liver transplantation. Delayed polymorphonuclear neutrophil apoptosis was related to the progression of acute lung injury. Inducing polymorphonuclear neutrophil apoptosis may help alleviate acute lung injury after orthotopic liver transplantation.
Postoperative pulmonary complications including acute lung injury (ALI) and acute respiratory distress syndrome have contributed to mortality and morbidity of orthotopic liver transplantation (OLT) with unclear mechanisms. Mast cells (MCs) and polymorphonuclear neutrophils (PMNs) are the main inflammatory cells and participants in the process of ALI. The present study was designed to investigate the role of MCs and PMNs and their potential relation to ALI following OLT. Rat orthotopic autologous liver transplantation (OALT) model was designed to determine lung injury at different time points after liver reperfusion. We also evaluated the function of MCs and the effect of tumor necrosis factor-a (TNF-a) and tryptase on AU and PMN apoptosis in rats subjected to OALT. Histological scores and inflammatory factor levels as well as PMN apoptosis were measured. Rats suffered from AU after OALT, which was demonstrated by a collapse of the pulmonary architecture, pulmonary edema, and infiltration of inflammatory cells in alveolar and interstitial spaces, as well as increased levels of proinflammatory cytokines. ALI maximized at 8 h after OALT. However, PMN apoptosis lagged behind the pulmonary injury and maximized at 16 h after OALT, when the acute inflammation resolution initiated. MC stabilization, and tryptase and TNF-alpha inhibitors could significantly decrease the lung pathophysiologic scores accompanied by an increase in PMN apoptosis. ALI after OALT was associated with MC activation and PMN apoptosis. ALI progression might be affected by delayed PMN apoptosis, which was related to MC activation. Induction of PMN apoptosis might alleviate ALI after OALT.
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