Genetic variation in neutrophil accumulation in mice is not mediated through immigrant regulatory cells.

Abstract

Genetic variation of induced peritoneal neutrophilia in mice was accompanied by parallel variation in macrophage responses. The timing of the macrophage responses in high responder (C57B1/10) mice indicated a potential role for these cells in mediating the enhanced neutrophil response. However, adoptive transfer of inflammatory macrophages did not induce neutrophilia. Analysis of peritoneal cytokine levels in high and low responder mice further indicated that IL-1, IL-3, GM-CSF, G-CSF and interferon-gamma (IFN-gamma) were not involved in mediating the genetic variation observed. Exogenous tumour necrosis factor-alpha (TNF-alpha) was effective in inducing the high responder phenotype, despite the absence of detectable TNF-alpha in either peritoneal fluid or serum. A role for genetically determined differential expression of endothelial adhesion molecules in high and low responders is suggested.