Tumor necrosis factor-alpha production after esophageal cancer surgery: differences in the response to lipopolysaccharide stimulation among whole blood, pleural effusion cells, and bronchoalveolar lavage fluid cells.

Abstract

The body's defense mechanism in response to stress may appear to be the sum of activation and suppression. We investigated chronological changes in tumor necrosis factor-alpha (TNF-alpha) production by local effusion cells and whole blood of esophageal cancer patients who had undergone radical resection. Whole blood, pleural effusion cells, and bronchoalveolar lavage fluid (BALF) cells were obtained from the 20 patients. Whole blood was stimulated with Escherichia coli (1 microg/ml), Staphylococcus aureus (10 microg/ml), and lipopolysaccharide (LPS) (1 microg/ml), and pleural effusion cells and BALF cells were stimulated with LPS; 24-H incubation and TNF-alpha concentration in supernate was measured by enzyme-linked immunosorbent assay (ELISA). Within 3 h after starting the operation, TNF-alpha production in whole blood was significantly (P < 0.05) decreased compared with preoperative value by each stimulation, and this suppression persisted up to day 3. These reductions in postoperative TNF-alpha production correlated with intraoperative hemorrhage. On the other hand, the LPS-induced release of TNF-alpha into pleural effusion cells and BALF cells were markedly increased during the study period. These results indicate that large quantities of cytokines are produced by a second attack, such as infection, in areas where immunocytes accumulate. We believe that the body reacts to surgical stress in a variety of ways. Circulating blood and immunocytes that accumulate in damaged organs are thought to react very differently to stress.