Thioglycollate-elicited murine macrophages are cytotoxic to Mycoplasma arginini-infected YAC-1 tumor cells

Macrophages are important components of natural immunity involved in inhibition of tumor growth and destruction of tumor cells. It is known that these cells can be activated for tumoricidal activity by lymphokines and bacterial products. We investigated whether YAC-1 tumor cells infected with Mycoplasma arginini stimulate nitric oxide (NO) release and macrophage cytotoxic activity. Thioglycollate-elicited macrophages from male BALB/c mice were co-cultured for 20 h with YAC-1 tumor cells infected or not with Mycoplasma arginini. The cytotoxic activity was evaluated by MTT assay and nitrite levels were determined with the Griess reagent. Thioglycollate-elicited macrophages co-cultured with noninfected YAC-1 cells showed low cytotoxic activity (34.7 ñ 8.6per cent) and low production of NO (4.7 ñ 3.1 µM NO2-). These macrophages co-cultured with mycoplasma-infected YAC-1 cells showed significantly higher cytotoxic activity (61.4 ñ 9.1 per cent; P=0.05) and higher NO production (48.5 ñ 13 µM NO2-; P=0.05). Addition of L-NAME (10 mM), an inhibitor of NO synthesis, to these co-cultures reduced the cytotoxic activity to 37.4 ñ 2per cent (P=0.05) and NO production to 3 ñ 4 µM NO2- (P=0.05). The present data show that Mycoplasma arginini is able to induce macrophage cytotoxic activity and that this activity is partially mediated by NO.

Paf antagonists do not modify IgE antibody production in mice

The effect of selective PAF antagonists on the in vivo production of IgE antibodies was investigated. The anti-ovalbumin IgE antibody content was estimated by passive cutaneous anaphylactic reaction (PCA) in the plasma of Balb/c mice 10 days after immunization with ovalbumin and alum. The PAF antagonists, BN 52021 (5 mg/kg, ip), BN 50730(20 mg/kg, ip) BN 50730 (20 mg/kg, po), WEB 2086 (2 mg/kg, ip) and WEB 2170 (5 mg/kg, ip) were administered 1 h before immunization and twice a day for 8 days thereafter. The effect of the antagonists on the PAF-induced vasopermeability was also assayed. In the immunized mice the level of antiovalbumin IgE antibody, estimated by PCA titer, was 1/640. The treatment with the PAF antagonists did not change this level. At the concentrations employed, the antagonists BN 50730, WEB 2086 and WEB 2170 significantly reduced the PAF-induced vascular permeability. These results suggest that PAF does not seem to have a relevant effect on the production of IgE antibodies in vivo in the system used in the present study

Involvement of eicosanoids and PAF in immune-coplex alveolitis

An immune-complex-mediated hypersensitivity reaction induced in the rat lung was followed by release of the eicosanoids thromboxane, prostaglandin E2 and leukotriene B4 into bronchoalveolar space. Concomitantly, there was a decrease in the number of circulating platelets. The thrombocytopenia was inhibited by a cyclo-oxygenase inhibitor (indomethacin), a platelet activating factor (PAF) antagonist (BN-52021) and an inhibitor of thromboxane (econazozle), but was not affected by a lipoxygenase inhibitor (NDGA). These results suggest the involvement of eicosanoids and PAF in the immune complex hypersensitivity reaction in the rat lung and indicate the ocurrence of interactions between PAF and thromboxane