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Role of protease-activated receptor 2 in lung injury development during acute pancreatitis in rats
Enrique de-Madaria1, María del Mar Francés, Sabrina Gea-Sorlí
1From the *Unidad de Gastroenterología, Hospital General Universitario de Alicante; †Instituto de Neurociencias, Universidad Miguel Hernández-Consejo Superior Investigaciones Científicas, Alicante; ‡Departamento de Patología Experimental, Instituto de Investigaciones Biomédicas de Barcelona-Consejo Superior Investigaciones Científicas, Insitut d'Investigacions Biomédiques August Pi i Sunyer, and Centro Investigación Biomédica en Red: Enfermedades Hepáticas y Digestivas, Barcelona; §Universidad Miguel Hernández, Elche; and ∥Centro Investigación Biomédica en Red: Enfermedades Neurodegenerativas, Madrid, Spain.
Objective:
The objective of this study was to evaluate whether an uncontrolled activation of mast cells and macrophages through protease-activated receptor-2 (PAR-2) during acute pancreatitis could develop lung injury.
Methods:
Pancreatitis was induced in rats by intraductal infusion of sodium taurocholate. In a group of animals, PAR-2 antagonist or trypsin (TRP) inhibitor was intravenously administered before the pancreatitis induction. In additional groups, the animals were treated with PAR-2-activating peptide or pancreatic TRP. The myeloperoxidase (MPO) activity was measured to evaluate the progression of inflammation.
Results:
Plasma from the animals with pancreatitis and pancreatic TRP induced the secretion of mast cells and alveolar macrophages as well as increased the density of PAR-2 in the plasma membrane. The treatment of alveolar macrophages with TRP, tryptase, as well as PAR-1- and PAR-2-activating peptide led to an increase in calcium-triggered exocytosis. Similar results were obtained in acinar cells. The intravenous injection of PAR-2-activating peptide and TRP induced an increase in MPO activity in the lung. The intravenous injection of PAR-2 antagonist or TRP inhibitor before the pancreatitis induction could prevent the increase in MPO activity in the pancreas and the lung.
Conclusions:
The TRP generated during acute pancreatitis could be involved in the progression of lung injury through the activation of PAR-2 in alveolar macrophages.
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