Alteration of surfactant proteins A and D in bronchoalveolar lavage fluid of Pneumocystis carinii pneumonia
- PMID: 11729507
Alteration of surfactant proteins A and D in bronchoalveolar lavage fluid of Pneumocystis carinii pneumonia
Abstract
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.
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