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Department of Surgery, University of Minnesota, Minneapolis, MN 55455
Evidence is provided that macrophages can make M-1 or M-2
responses. The concept of M-1/M-2 fomented from observations that
macrophages from prototypical Th1 strains (C57BL/6, B10D2) are more
easily activated to produce NO with either IFN-
or LPS than
macrophages from Th2 strains (BALB/c, DBA/2). In marked contrast, LPS
stimulates Th2, but not Th1, macrophages to increase arginine
metabolism to ornithine. Thus, M-1/M-2 does not simply describe
activated or unactivated macrophages, but cells expressing distinct
metabolic programs. Because NO inhibits cell division, while ornithine
can stimulate cell division (via polyamines), these results also
indicate that M-1 and M-2 responses can influence inflammatory
reactions in opposite ways. Macrophage TGF-ß1, which inhibits
inducible NO synthase and stimulates arginase, appears to play an
important role in regulating the balance between M-1 and M-2. M-1/M-2
phenotypes are independent of T or B lymphocytes because C57BL/6 and
BALB/c NUDE or SCID macrophages also exhibit M-1/M-2. Indeed, M-1/M-2
proclivities are magnified in NUDE and SCID mice. Finally, C57BL/6 SCID
macrophages cause CB6F1 lymphocytes to increase
IFN- production, while BALB/c SCID macrophages increase TGF-ß
production. Together, the results indicate that M-1- or M-2-dominant
macrophage responses can influence whether Th1/Th2 or other types of
inflammatory responses occur.
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D. H. Dockrell, H. M. Marriott, L. R. Prince, V. C. Ridger, P. G. I |
