Abstract
Goal: to evaluate the effect of induced immunosuppression on the nature and speed of structural-functional disturbances formation in the lungs on the COPD model.
Methods: The COPD model was created in Wistar rats by exposure with nitrogen dioxide (NO2, 15-19 ppm): three 30-minute exposures per day with 30 min intervals for 60 days. To create immunosuppression, an alkylating agent cyclophosphamide was injected intraperitoneally twice, the control group got 0.9% NaCl. BAL fluid cytogram was determined. The presence of IL-8, IL-17, neutrophil elastase (NE), sIgA, SP-D in BAL fluid was measured by ELISA method. Histological preparations were stained with H&E.
Results: Immunosuppression contributed to an earlier and pronounced activation of the inflammatory process in comparison with the control. By the 30th day of NO2 exposure, the neutrophil content in BALF increased to 31.4±2.8% (in control, 22.3±1.7%, p<0.05); TNFα-up to 35.48±2.08 vs 25.45±1.33 pg/ml in control, p<0.05; IL-8-up to 39.79±1.12 vs 30.28±1.09 pg/ml, p<0.05; NE-32.74±1.77 vs 21.76±1.98 ng/ml, p<0.05; IL-17-76.53±4.85 vs 69.47±3.37 pg/ml, p<0.05. Levels of bronchial epithelium functional activity markers (SP-D, sIgA) decreased (p<0.05). In distinction from the control group, signs peculiar to COPD model, were detected after 30 (in control after 60 days) from the onset of NO2 exposure.
Conclusion: When aggressive pollutants damaging the respiratory epithelium are exposed, the initial immune dysfunction maycontribute to the formation of a pro-inflammatory environment and the phenotype of premature lungs aging, predisposing to the development of chronic obstructive pulmonary pathology.
Footnotes
Cite this article as: European Respiratory Journal 2019; 54: Suppl. 63, PA3853.
This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).
- Copyright ©the authors 2019