Control of complement synthesis and secretion in bronchoalveolar and peritoneal macrophages.

The effect of inflammation on C (C2 and C4) biosynthesis by bronchoalveolar and peritoneal cells was studied with methods that detect changes in synthesis rates and qualitative changes in cell populations. Adherent bronchoalveolar macrophages produced less C2 and C4 than adherent peritoneal macrophages. However, the subset of cells capable of producing C was more than 20-fold greater in the peritoneal cell population than in the population of bronchoalveolar cells. The rate of synthesis per C producing bronchoalveolar macrophage was 5 to 10 times the rate by C producing peritoneal macrophages. In contrast, the effect of an inflammatory stimulus on C production was the result of a change in rate of synthesis per cell, not a change in the proportion of C producing cells. This stimulatory effect was exerted locally, not on a cell population harvested from a distant site. At least two mechanisms for local control of C levels in tissues have been identified--that is, a change in synthesis rate and a qualitative change in macrophage cell population. The capacity to alter C levels at a site of inflammation may be important for C dependent functions in host defenses.