Do type III interferons play a role in bronchopulmonary dysplasia? 4248

Abstract Description Bronchopulmonary Dysplasia (BPD) is the most common complication associated with prematurity. It is characterized by an arrest of lung development due to inflammatory responses induced by oxidative stress caused primarily by mechanical ventilation and oxygen supplementation. However, the mechanisms linking oxidative stress and pulmonary inflammation remain poorly understood. Recent studies have shown that type I and III interferons (IFN-I and IFN-III) disrupt lung epithelial barrier and repair process during viral infection. However, the role of IFN-III in BPD is still unknown. In this study, we aimed to assess the effects of hyperoxia on IFN-I/III production and its effects on alveolar epithelial cell (AECs) functions. For this, we used in vivo (mouse) and in vitro (AECs cell line) models of hyperoxia (>95% O2) compared to normoxia (21% O2). We found that while hyperoxia had no effects on IFN-I levels, we observed a significant increase in IFN-III production by AECs. We also found that hyperoxia reduced AECs proliferation even after return to normoxia, a feature of cellular senescence. We envision that blocking IFN-III or its receptor will reverse this phenotype. Thus, our results provide new insights into a potential novel therapeutic target for BPD. Topic Categories Immune Response Regulation: Cellular Mechanisms (IRC)