POSSIBLE PARTICIPATION OF MACROPHAGE INFLAMMATORY PROTEIN-2 IN NEUTROPHIL INFILTRATION IN ALLERGIC INFLAMMATION IN RATS

Recombinant rat macrophage inflammatory protein 2 (MIP-2) was prepared from E, coli transfected with a glutathione-S-transferase (GST)-MIP-2 fusion protein expression vector. A polyclonal antibody to rat MIP-2 was then obtained from rabbits by immunization with recombinant rat MI P-2. Using the polyclonal antibody which selectively suppressed neutro phil chemotactic activity of MIP-2, the role of MIP-2 in neutrophil in filtration in allergic inflammation in rats was studied. In an air pou ch-type allergic inflammation model in rats, neutrophil infiltration i nto the pouch fluid increased with time after antigen challenge. Neutr ophil chemotactic activity in the pouch fluid collected 8 h after anti gen challenge was diminished by anti-MIP-2 antibody. In addition, when leukocytes that had infiltrated into the pouch fluid collected 4 h af ter antigen challenge were incubated, neutrophil chemotactic activity in the conditioned medium increased time-dependently, and the activity was neutralized by anti-MIP-2 antibody. Furthermore, when anti-MIP-2 antibody was injected into the pouch 6 h after antigen challenge, neut rophil infiltration into the pouch fluid during the next 2 h was suppr essed. These findings indicate that MIP-2 plays an important role in n eutrophil infiltration in rat allergic inflammation. (C) 1997 Elsevier Science B.V.