[Production of chemokines by the human peritoneum]

Peritonitis is characterised by a continued infiltration of the peritoneal cavity with leukocytes, attracted by chemotactic mediators. The aim of this study was to demonstrate the capacity of the human peritoneum to secrete chemokines and to show a therapeutic option by impairing the proinflammatory function of the peritoneum.

Peritoneum was obtained from 12 consenting patients undergoing abdominal surgery for noninflammatory diseases. After opening the peritoneal cavity a piece of the parietal peritoneum was excised and subsequently incubated with lipopolysaccharide (LPS, 50 ng/ml) +/- interleukin-10 (IL-10, 100 U/ml) for five hours in vitro. The culture supernatants were assayed for concentrations of interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1) and monocyte inflammatory protein-1 alpha (MIP-1 alpha) by using the ELISA.

The cultured peritoneum secreted MCP-1 (mean (SEM): 3416 (659) pg/ml) and IL-8 (2946 (894) pg/ml). The presence of LPS resulted in a fourfold enhancement of this secretion (MCP-1: 13563 (1613), IL-8: 9854 (1305) pg/ml) and led to the production of MIP-1 alpha (1476 (240) pg/ml). The LPS-stimulated production of all of these chemokines was significantly diminished by the presence of IL-10.

The reaction of the peritoneum to LPS indicates its proinflammatory function in the context of peritonitis caused by gram-negative bacteria. This inflammatory reaction might be diminished by application of IL-10.