A new understanding of pancreatitis-associated pulmonary injury

Abstract

Pancreatitis-associated lung injury (PALI) is one of the earliest organ dysfunctions occurring in patients with severe acute pancreatitis. In this review we explore potential mechanisms of endothelial barrier dysfunction, neutrophil and monocyte/ macrophage activation, adhesion molecule expression, initial factors, mast cell involvement and intracellular signaling in PALI. Different regulatory mechanisms exist in PALI and sepsis-induced lung injury. Endothelial barrier dysfunction occurs early on in acute pancreatitis and tumor necrosis factor (TNF)-a and monocyte chemoattractive protein-1 levels in the circulation gradually increase in acute pancreatitis. Leukocytes from the circulation, lung tissue and bronchoalveolar fluid exhibit different expression and activation patterns in the development of PALI. Mast cells seem to be involved in the initiation of leukocyte activation during the initial phase of PALI. Activation of the protein kinase C (PKC) signaling pathway could play an important role in the pathogenesis of PALI. Inhibition of PKC may be one candidate to prevent and treat the development of PALI.