Compartmental Apoptosis and Neutrophil Accumulation in Severe Peritonitis

Background Migration and activation of polymorphonuclear neutrophils (PMN) and apoptosis are central to inflammatory tissue damage This study examines the relation of these processes, and their expression in the abdominal, systemic, and bronchoalveolar compartments in patients with severe peritonitis Materials and Methods Thirty one consecutive patients undergoing laparotomy for severe secondary peritonitis Eight operated patients without peritonitis and 10 long-term mechanically ventilated noninfected patients served as controls Peritoneal fluid, blood, and bronchoalveolar lavage fluid (BALF) was obtained on d 0 (day of initial laparotomy), 2, and 3 Levels of chemokines (interleukin (IL) 8 and monocyte chemotactic protein (MCP)-1), PMN counts, PMN activation [myeloperoxidase (MPO), elastase] and apoptosis (nucleosomes) were determined Results In peritonitis patients, levels of chemokines and markers of PMN sequestration were in creased in all compartments IL-8 levels were higher in BALF than in plasma, and did not originate from the circulation or from lysis of alveolar cells Pulmonary nucleosome levels were higher in patients who died (P = 0 020), and corresponded with PMN count in BALF (P <0 001), levels of chemokines (IL 8, P = 0 003, MCP-1, P = 0 001), and PMN activation (MPO, P <0 001, elastase P = 0 007) Conclusion Severe peritonitis produces an early pulmonary expression of chemoattractants creating a gradient for PMN sequestration and activation into the lung These parameters are associated with expression of apoptosis in the lung, which is increased in non surviving peritonitis patients (C) 2010 Elsevier Inc All rights reserved