Abstract

Previously, we reported differences in arachidonic acid metabolism in elicited chicken peritoneal macrophages when compared with murine resident and elicited peritoneal macrophages.¹ We now describe leukotriene (LT) production in the same systems, using resident (murine) and inflammatory macrophages (from both species). Inflammatory (4- or 42-h Sephadex-elicited) peritoneal macrophages from chickens lacked the capacity to produce LT in vivo (following opsonized zymosan [OZ] stimulation) or in vitro, in response to A23187. In addition, chicken macrophages were unable to metabolize exogenously added LTC₄ or LTD₄ in vitro. In contrast, resident murine peritoneal macrophages produced measurable quantities of LTs (in vivo) within 5 min with an 8-fold increase after 45 min. LTC₄ was effectively converted to LTE₄ in vivo in a time-dependent manner (65% LTC₄/35% LTE₄ after 5 min stimulation with OZ and 6% LTC₄/94% LTE₄ after 60 min stimulation), but not in vitro. The lack of LTC₄ metabolism to LTE₄ in vitro could not be explained by cell-cell interaction between adherent and nonadherent cells. LTD₄ was not detected under any experimental condition. Murine peritoneal cells incubated with LTD₄ (with or without agonist) produced LTE₄ in a time-dependent fashion. Addition of -cysteine (a dipeptidase inhibitor) did not explain the lack of detectable levels of LTD₄ following intraperitoneal stimulation with OZ. These results suggest that elicited chicken peritoneal macrophages are incapable of producing LTs compared to murine peritoneal macrophages. In addition, these studies fail to explain the different product profiles associated with in vivo stimulation of murine peritoneal macrophages as compared to in vitro stimulation.

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Corresponding author. Correspondence to: Dr Jay Whelan, Department of Nutrition, 229 Jessie Harris Building, University of Tennessee, Knoxville, TN 37996-1900.