Alteration of surfactant proteins A and D in bronchoalveolar lavage fluid of Pneumocystis carinii pneumonia.

OBJECTIVE

To understand the interaction between surfactant proteins and pneumocystis carinii pneumonia (PCP), and the impact of corticosteriods on surfactant proteins.

METHODS

We established rat models of PCP and bacterial pneumonia induced by subcutaneous injection of 25 mg cortisone acetate. At 8-12 wk, the bronchoalveolar lavage fluid (BALF) of rats was collected. Total nucleated cells of BALF were counted and differentiated, and the concentrations of surfactant protein A (SP-A) and surfactant protein D (SP-D) were measured by immunoblotting assay. The rats were divided into three immunosuppressive groups and a normal control group. Group I, normal control (n = 6), consisted of healthy SD rats; group II, negative control (n = 6), consisted of rats with cortisone acetate injection for over 8 wk without lung infection; group III, bacterial pneumonia (n = 11), rats were injected with cortisone acetate over 8 wk that resulted in bacterial pneumonia without other pathogens isolated; and group IV, PCP (n = 14), rats with injected cortisone acetate for 8-12 wk and developed PCP without other pathogens isolated.

RESULTS

Our results indicated that the total cell count in BALF in the negative control group was lower than that in the normal control group (P < 0.001). During PCP infection, the total cell count and the percentage of polymorphonuclearcytes (PMNs) in BALF were significantly increased (P < 0.01), but were lower than those in the bacterial pneumonia group. The concentration of SP-A of BALF in PCP (45.1 +/- 22.1 micrograms/ml) was significantly increased in comparison with that in the negative control (16.2 +/- 9.9 micrograms/ml, P < 0.05) and bacterial pneumonia groups (6.2 +/- 5.6 micrograms/ml, P < 0.001). We also found that the relative content of SP-D was significantly higher in PCP (24,249 +/- 4780 grey values) than that in the negative control (13,384 +/- 2887 grey values, P < 0.001) and that in bacterial pneumonia (11,989 +/- 2750 grey values, P < 0.001). SP-A and SP-D were also higher in the moderate to heavy group of PCP than those seen in the mild group (P < 0.01, P < 0.001). SP-A and SP-D were higher in the negative control group than those in the normal control group, but there was no significant difference between the 2 groups.

CONCLUSION

These results suggest that the concentrations of SP-A and SP-D in BALF are increased by pneumocystis carinii specific stimulation, but the alteration is not related to the corticosteriod usage.