Document Type : Original Article
IMMUNOLOGY DEPARTMENT AND RESEARCH CENTER OF MOLECULAR BIOLOGY, BAQIYATALLAH MEDICAL SCIENCES UNIVERSITY, TEHRAN, IRAN
Introduction: It has been shown that gama-IFN is one of the major cytokines involved in lung fibrosis. It has also been demonstrated that Nitric Oxide (NO) may exert vasodilation, edema and cytotoxicity, and it may stimulate cytokinedependent processes in the lungs. In this study, the effect of 17-beta Estradiol (17-betaE2) and five alpha dihydrotestosterone (5alfa-DHT) on NO release by TGF beta treated alveolar macrophages was investigated.
Material and Methods: Alveolar macrophages were obtained by bronco alveolar lavage of healthy male rats aged 8 to 10 weeks in the usual manner. Lavaged cells (95% alveolar macrophages) were plated out at 1x105 cells/well using a 24 well flat bottomed cell culture plate. Cells were incubated for 2hrs at 37°C and 5% CO2. Non adherent cells were removed by three washings and alveolar macrophages were covered with 1 ml complete medium without phenol Red containing 10 µg/ml LPS,100U gama-IFN and different concentration of 17beta E2 or 5alfa-DHT in the presence or absence of TGF beta. Cells were incubated for another 24h and supernatants were collected and Nitrite was measured using indicator of NO by Griess method.
Results: Results showed that TGF-beta reduced 5alfa-DHT induced NO release. The minimum and maximum reduction in NO release was seen in response to 1x10-10M to 1x10-6M, indicating that TGF-beta was able to reduced 5alfa-DHT induced NO. It also showed that 17beta E2 reduced NO release in TGF-beta treated macrophages in a dose dependent fashion. The minimum and maximum inhibition in NO release was seen in response to 1x10-11M and 1x10-6M respectively.
Conclusion: According to results it seems that the part of pulmonary inflammation which is related to TGF-beta probably due to nitric oxide release and that sex hormones may play a role in this process.