The purpose of this study was to determine if the secretion of cytotoxic molecules, such as tumor necrosis factor or toxic oxygen molecules, by resident peritoneal macrophages is modulated by postsurgical macrophages elicited by peritoneal trauma. Resident macrophages were collected from nonsurgical rabbits and cultured in vitro with either spent media from cultures of postsurgical macrophages harvested at various times or with varying concentrations of standard cytokines. Superoxide anion (O2/-) production of resident macrophages increased with exposure to spent culture media from macrophages obtained after intestinal reanastomosis (3, 6, 12, 24 hr). This increase reached maximal levels by 6 hr after surgery and thereafter decreased to resident levels by 24 hr after surgery. Exposure of resident macrophages to spent media from cells collected after peritoneal sidewall abrasion (1, 3, 5, 7, 10, 14 days) elevated the production of O2/- on Postsurgical Days 3 and 5; however, no effect was observed following exposure to spent media of macrophages harvested on Postsurgical Day 14. Interleukin-1α (IL-1α), transforming growth factor β (TGF-β), and tumor necrosis factor α (TNFα) stimulated phorbol ester-induced O2/- production by resident macrophages in a concentration-dependent manner. The secretion of TNF activity by resident macrophages increased following exposure to spent media of macrophages harvested 6 to 24 hr after intestinal surgery. IL-1α, TGF-β, and TNFα elevated the secretion of TNF activity by resident macrophages in a concentration-dependent manner. However, no effects on O2/- production nor TNF secretion were observed using other cytokines, including interleukin-2, fibroblast growth factor, epithelial growth factor, insulin, and insulin-like growth factor. Our data suggest that peritoneal resident macrophages could be primed by soluble factors produced by postsurgical macrophages, such as IL-1α and TNFα, and those factors could change macrophage cytotoxic activity as a function of postsurgical time.
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