In vivo inhibition of granulopoiesis in acute inflammation requires T lymphocyte integrity

In previous studies, we have shown that mice undergoing an inflammatory reaction induced by subcutaneous (s.c.) implantation of copper rods elaborate humoral factors that initially enhance, and subsequently inhibit, diffusion chamber (DC) granulopoiesis. In order to quantify the inhibition of DC granulopoiesis after inflammation, one to three copper rods were implanted s.c. either at the same place (1 abscess), or at different sites (multiple abscesses). There was an inverse relationship between the increase in the number of abscesses, and the number of DC granulocytic cells measured in the inhibitory phase. To investigate the role of T lymphocytes in the release of putative inhibitory factor(s) that act on DC cells, cyclosporin A (CyA), a T lymphocyte function inhibitor, was given orally each day (0.75 mg) to mice, starting two days before copper implantation. CyA abrogated the inflammation-related inhibition on DC spleen colony-forming units (CFU-s), granulocyte-macrophage colony-forming units (CFU-gm), and total cell production. To confirm these results, DC were implanted in T cell deficient nude mice where no inhibition of DC cells was observed after inflammation. In conclusion, our data suggest that the in vivo inhibition of granulopoiesis is related to the level of the inflammatory stimulus and requires the functional integrity of T cells.