In vivo regulation of granulocyte protluction in acute inflammation

Abstract

In order to study in vivo the enhanced granulopoiesis that occurs during acute inflammation, 1-3 sterile metallic copper rods were inserted subcutaneously into mice either at the same place (one abscess) or at different sites (multiple abscesses). Diffusion chambers filled with bone marrow cells were implanted intraperitoneally for 3 days. When a single abscess was created, the granulocytic content of the diffusion chamber increased similarly whatever the number of inserted copper rods. However, there was a direct relationship between the number of abscesses and the number of granulocytic cells harvested from the diffusion chambers. In order to investigate the role of T-lymphocytes in the production of diffusible stimulating factors that act on diffusion chamber granulopoiesis, cyclosporin A (CyA) was given to the mice with implanted copper rods. CyA abrogated the induced enhancement of CFU-S, CFU-GM and mature granulocyte numbers inside the diffusion chamber. The stimulatory effect of inflammation on diffusion chamber granulopoiesis was not observed in T-lymphocyte-deficient nude mice. These data suggest that in vivo stimulation of granulopoiesis is related to the level of inflammation, and that this effect requires the functional integrity of T-lymphocytes.

Contribution of Lymphocytes in Edema Induced by Venom from the Wasp (Belonogaster fuscipennis)

“…This is because amethopterin-induced leucopenia reduced the experimental edema evoked by phospholipase A2 from Trimeresurus mucrosquamatous venom (Wang & Teng, 1992). The response of the granulocytes inflammation appears to require the functional intergrity of the lymphocytic series (Hamood & Fondu, 1991), therefore, a complex regulated system involving haematogenous cells is likely to play a role in venom-induced lesions (Cury et al, 1994).…”