Effects of corticosteroids and cyclophosphamide on a mouse model of Chlamydia trachomatis pneumonitis.
Suppression of the inflammatory reaction with daily doses of cortisone acetate or cyclophosphamide substantially prolonged the pulmonary infection in mice which had been intranasally inoculated with a trachoma biotype of Chlamydia trachomatis. Titration of organisms recovered from the lungs of treated mice revealed a drop in titer after day 2 (postinfection), followed by a prominent increase on day 6. In cyclophosphamide-treated mice the infection was resolved after day 12, whereas in cortisone acetate-treated mice a significant titer remained after day 17. In contrast, no organisms were recoverable after day 6 in control mice treated with saline or in mice treated with hydrocortisone succinate. Histologically, the ability of cortisone acetate and cyclophosphamide to inhibit the inflammatory reaction correlated with the respective course of chlamydial pneumonitis. This study demonstrated that mice were intrinsically capable of sustaining a lung infection induced by a human strain of S. trachomatis.
D000818:Animals; D002690:Chlamydia Infections / Q000382:microbiology* / Q000473:pathology; D002691:Chlamydophila psittaci / Q000254:growth & development*; D003348:Cortisone / Q000031:analogs & derivatives* / Q000494:pharmacology; D003520:Cyclophosphamide / Q000494:pharmacology*; D006854:Hydrocortisone / Q000031:analogs & derivatives / Q000494:pharmacology; D007958:Leukocyte Count; D008168:Lung / Q000382:microbiology / Q000473:pathology; D008297:Male; D051379:Mice; D011014:Pneumonia / Q000382:microbiology* / Q000473:pathology; D013997:Time Factors
D003520:Cyclophosphamide; C007133:hydrocortisone hemisuccinate; D003348:Cortisone; D006854:Hydrocortisone