Department of Physiology and Pathophysiology, University of Manitoba, Canada; Biology of Breathing Group, Children's Hospital Research Institute of Manitoba, Canada.
Department of Physiology and Pathophysiology, University of Manitoba, Canada; Biology of Breathing Group, Children's Hospital Research Institute of Manitoba, Canada.
Int J Biochem Cell Biol. 2020 Dec;129:105864. doi: 10.1016/j.biocel.2020.105864. Epub 2020 Oct 15.
Oxidative stress is an important feature of asthma pathophysiology that is not currently targeted by any of our frontline treatments. Reactive oxygen species, generated during times of heightened oxidative stress, can damage cellular lipids causing the production of oxidation specific epitopes (OSE). OSEs are elevated in chronic inflammatory diseases and promoting their clearance by the body, through pattern recognition receptors and IgM antibodies, prevents and resolves inflammation and tissue damage in animal models. Current research on OSEs in asthma is limited. Although they are present in the lungs of people with asthma during periods of exacerbation or allergen exposure, we do not know if they are linked with disease pathobiology. This article reviews our current understanding of OSEs in asthma and explores whether targeting OSE clearance mechanisms may be a novel therapeutic intervention for asthma.
氧化应激是哮喘病理生理学的一个重要特征,但目前我们的一线治疗方法都没有针对这一特征。在氧化应激加剧时产生的活性氧会破坏细胞脂质,导致氧化特异性表位(OSE)的产生。OSE 在慢性炎症性疾病中升高,通过模式识别受体和 IgM 抗体清除它们,可以预防和解决动物模型中的炎症和组织损伤。目前关于哮喘中 OSE 的研究有限。尽管在哮喘患者哮喘发作或过敏原暴露期间肺部存在 OSE,但我们尚不清楚它们是否与疾病发病机制有关。本文综述了我们目前对哮喘中 OSE 的认识,并探讨了针对 OSE 清除机制是否可能成为哮喘的一种新的治疗干预措施。