In vivo elaboration of CSF in acute inflammation: proportionality to the intensity of the inflammatory stimulus and requirement of T lymphocytes.

The colony-stimulating factor(s) (CSF) that stimulates the in vitro growth of bone marrow granulocyte-monocyte progenitors (CFU-GM) increases in the serum of mice challenged by an aseptic abscess induced by copper rod insertion. The effect of the inflammation on the increase of serum CSF is dose-related. The creation of 3 aseptic abscesses indeed results in a higher and longer elevation of serum CSF than 1 abscess. Serum CSF also increases in parallel with the rise in bone marrow CFU-GM; this is consistent with the CSF playing a role in regulation of haematopoiesis in vivo. From previous studies, it appears that T lymphocytes play a central role in the regulation of haematopoiesis. In order to determine the role of T lymphocytes in the inflammation response, cyclosporin A (CyA), an inhibitor of T lymphocyte function, was given in vivo, 2 days before inflammation induction. CyA abrogates the increase in both serum CSF and CFU-GM. Furthermore, a lower increase in serum CSF was observed in copper-implanted nude mice. These results suggest that the CSF production induced by inflammation requires the functional integrity of T lymphocytes.