The specific activity of phospholipase A 2 (PLA 2) in the liver homogenate was elevated 1.7-fold in bacillus Calmette-Guerin (BCG)-treated rats, 1.6-fold in lipopolysaccharide (LPS)-treated rats, and 2.4-fold in BCG-infected rats treated with LPS, compared with that of control rats. These increased activities were almost completely inhibited by the antibody directed against rat splenic group II PLA 2 (PLA 2M) but not by anti-pancreatic PLA 2 antibody. The results of immunoblot analysis confirmed that the PLA 2 immunochemically related to the group II enzyme was induced by treatment with BCG and/or LPS. The anti-PLA 2M antibody-inhibitable PLA 2 activity per a single cell was elevated not only in nonparenchymal cell fraction but also in hepatocyte fraction, as in the case of whole liver. On the contrary, the PLA 2 concentration and its specific activity did not change by the same treatment both in spleen homogenate and in isolated spleen cell fractions although a 3-fold increase in spleen mass occurred by BCG treatment. These results suggested that a tissue-specific mechanism of the PLA 2 induction by these inflammatory mediators may operate in liver.