In order to induce heavy Pneumocystis pneumonia, rats were treated with dexame-, thasone twice a week for 14 weeks. Mature cysts, immature cysts and ruptured cysts were, identified on lung imprints. By phase-contrast microscopy mature cysts were spherical in, shape containing intracystic bodies both spherical and irregular, small to large trophozoites having polymorphic shapes, one nucleus and many vacuoles. Elcctro-microscopically, large amount of irregular trophozoites adhered to the surface of the type I alveolar epithelial cells in the alveolar cavity were observed. The above histological findings were typical features of Pneumocystis pneumonia (Figs. 1-8).

Objective To study the effect of IL-12 on Th1/Th2 cytokine expression level and the role of IL-12 in the shi ft ing of Th1/Th2 immune response against blood-stage Plasmodium b e ighei infection in mice. Methods [WT5”BZ ]BALB/c mice were infected with 5?105 parasitized RBC and received doses of 0.03 or 0.15 ?g/d of IL-12 on the day of infection and daily for 6 days post -in fection. The levels of IFN-? and IL-4 in sera or supernatants of splenic lymp hocyte cultured in vitro were detected by the EL ISA method. Results Compared with spleen cells fro m untreated mice, spleen cells from 0.03 ?g dose of IL-12-treated mice produ ced significantly higher level of Th1-associated cytokine IFN -?, but lower level of Th2-associated cytokine IL-4 in response to PHA or sA g stimulation on day 7 post-infection, whereas spleen cells from 0.15 ?g dose I L-1 2-treated mice produced significantly lower levels of IFN-? and IL-4. The le vel of IFN-? was apparent in the sera of mice treated with 0.03 or 0.15 ?g/d I L-12 on day 3 post-infection and peaked on the day 5 post-infection, but level of I FN-? even was significantly lower in mice treated with 0.15 ?g/d IL-12 comp ara ble to that in control mice on day 7 post-infection. The level of IFN-? was n ot detected in the sera of control mice through 7 days post-infection. [WT5” H Z] Conclusion Appropriate dose of IL-12 regulates the deve lop ment of resistance to P.berghei via a CD 4+ T h1 response, which involves the cytokines IFN-?. [HT5”SS] However, higher doses of IL-12 dramatically inhibite immune pro t ective ability, which may be detrimental to resistance against P .berghei infection. [