Surfactant phospholipids and lavage phospholipase A2 in experimental Pneumocystis carinii pneumonia.
The effect of Pneumocystis carinii pneumonia on surfactant phospholipids and lavage phospholipase A2 was investigated. Pneumocystis carinii infection was induced in adult rats by immunosuppression with dexamethasone administered in the drinking water (2 mg/L) for 6 to 8 wk. Surfactant phospholipids were isolated from lung lavage and lung tissue. Dexamethasone administration significantly increased total lung and lavage phospholipids in corticosteroid-treated animals receiving prophylaxis against P. carinii with trimethoprim-sulfamethoxazole (TMP-SMZ) when compared with no treatment control animals. Lavage surfactant phospholipids from P. carinii-infected rats were 25% that of no treatment control rats and less than 10% that of corticosteroid control animals receiving TMP-SMZ. Phospholipid composition of lavage phospholipids was also altered in P. carinii pneumonia, with slight increase in the percentage of sphingomyelin and reduced percentage of total phosphatidylcholine. Postlavage tissue phospholipids of P. carinii-infected rats were 4 times that of no treatment control animals, although only about 50% that of corticosteroid control animals. There was no significant difference in lavage phospholipase A2 activity for the P. carinii-infected and corticosteroid control groups, although the enzyme activity was at least 4 times that of the no treatment control group. The surfactant changes were associated with abnormal excised lung pressure-volume curves and decreased deflation stability in the animals with P. carinii. These results indicate that the corticosteroids used in this model induce an increase in both lung surfactant phospholipids and phospholipase A2. Despite this increase in lavage phospholipids, P. carinii pneumonia in this model causes an alveolar surfactant phospholipid deficiency without significant increase in phospholipase A2 activity.(ABSTRACT TRUNCATED AT 250 WORDS)
D000818:Animals; D000890:Anti-Infective Agents / Q000627:therapeutic use; D003907:Dexamethasone / Q000494:pharmacology; D004338:Drug Combinations / Q000627:therapeutic use; D007165:Immunosuppression Therapy; D008168:Lung / Q000378:metabolism* / Q000473:pathology; D008244:Lysophosphatidylcholines / Q000378:metabolism; D008297:Male; D009929:Organ Size; D010714:Phosphatidylethanolamines / Q000378:metabolism; D010715:Phosphatidylglycerols / Q000378:metabolism; D010740:Phospholipases / Q000378:metabolism*; D010741:Phospholipases A / Q000378:metabolism*; D054467:Phospholipases A2; D010743:Phospholipids / Q000378:metabolism*; D011020:Pneumonia, Pneumocystis / Q000378:metabolism* / Q000473:pathology / Q000517:prevention & control; D011663:Pulmonary Surfactants / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D013420:Sulfamethoxazole / Q000627:therapeutic use; D007507:Therapeutic Irrigation; D014295:Trimethoprim / Q000627:therapeutic use; D015662:Trimethoprim, Sulfamethoxazole Drug Combination
D000890:Anti-Infective Agents; D004338:Drug Combinations; D008244:Lysophosphatidylcholines; D010714:Phosphatidylethanolamines; D010715:Phosphatidylglycerols; D010743:Phospholipids; D011663:Pulmonary Surfactants; D003907:Dexamethasone; D015662:Trimethoprim, Sulfamethoxazole Drug Combination; D014295:Trimethoprim; D010740:Phospholipases; D010741:Phospholipases A; D054467:Phospholipases A2; D013420:Sulfamethoxazole