Effects of impaired glucocorticoid receptor function in hemorrhagic shock-induced lung injury with pre-existing cigarette smoke-induced chronic obstructive pulmonary disease (B07*)

当小鼠接受重症监护治疗时，我们发现缺乏GR二聚化（GRdim）会增加死亡率，加重低血压，并在脂多糖激发后进一步损害肺功能。因此，B07 N假设，在GRdim小鼠中，失血性休克后的肺损伤和全身炎症加剧，这进一步被创伤前香烟烟雾吸入诱导的COPD所促进。我们预计糖皮质激素（GC）治疗通过协同基因诱导改善肺功能并减少炎症，这是由替代巨噬细胞中依赖于GRdim的炎症和抗炎作用信号通路促进的。

When mice receive intensive care treatment, we found that a lack of GR dimerization (GRdim) increases mortality, aggravates hypotension, and further impairs lung function after challenge with lipopolysaccharides. Therefore, B07 N hypothesizes that lung injury and systemic inflammation after hemorrhagic shock are exacerbated in GRdim mice, which is further promoted by pre-traumatic cigarette smoke exposure-induced COPD. We expect that glucocorticoid (GC) treatment improves lung function and reduces inflammation through synergistic gene induction, which is promoted by inflammatory- and anti-inflammatory-acting signaling pathways dependent on GRdim in alternative macrophages.