İmmunohistochemical detection of IL-1, SP-A expression in lungs of Brucella melitensis infected ovine fetuses

It has been reported that maternal intrauterine infections can affect organs such as lungs and brain by causing a systemic inflammation and increase in cytokines in the fetus, and play an important role in the development of lung damage and bronchopulmonary dysplasia (BPD). In this study, the effects of proinflammatory cytokines IL-1β and antiinflammatory cytokines IL-10 and SP-A on lung damage in fetuses were evaluated by immunohistochemical staining in 30 sheep aborted fetus lungs in a naturally infected intrauterine infection model with B. melitensis. It was determined that the most affected tissue in sheep fetus histopathologically was lung. Bronchopneumonia was observed in 12 fetuses (40%) in the lung. An increase in the interalveolar and interlobular area was detected in 18 (60%) cases. In the immunohistochemical examination, Brucella melitensis antigen was intensely stained in the lungs, especially in the cytoplasm of alveolar macrophages. IL-1 was immunopositive with varying severity in alveolar macrophages, endothelial cells and bronchial-bronchiol epithelial cells in all fetal lungs (100%). The anti-inflammatory cytokine IL-10 was only slightly stained in the fetal lung tissue, alveolar macrophages, and bronchial and bronchiole epithelial lumen in three (10%) cases. SP-A positive immunoreactivity was detected in type II pneumocytes of fetal lungs and alveolar lumens in 5 (16%) cases. It was determined that the proinflammatory cytokine IL-1 gave intense immunoreactivity in the damaged infected lung tissues, while the expression of the anti-inflammatory cytokine IL-10 was found to be significantly lower when compared to the healthy control fetus lungs. It was thought that lung damage in intrauterine infections was caused by the increase in the balance of cytokines, the amount of proinflammatory cytokine IL-1, and the positive reaction of SP-A in only 5 cases was due to the early gestational age, therefore the lungs of the fetuses have not yet completed their development and type II pneumocytes have not developed.