Oxidative stress diseases unique to the perinatal period: A window into the developing innate immune response.
Robert M DietzClyde J WrightPublished in: American journal of reproductive immunology (New York, N.Y. : 1989) (2017)
The innate immune system has evolved to play an integral role in the normally developing lung and brain. However, in response to oxidative stress, innate immunity, mediated by specific cellular and molecular programs and signaling, contributes to pathology in these same organ systems. Despite opposing drivers of oxidative stress, namely hyperoxia in neonatal lung injury and hypoxia/ischemia in neonatal brain injury, similar pathways-including toll-like receptors, NFκB and MAPK cascades-have been implicated in tissue damage. In this review, we consider recent insights into the innate immune response to oxidative stress in both neonatal and adult models to better understand hyperoxic lung injury and hypoxic-ischemic brain injury across development and aging. These insights support the development of targeted immunotherapeutic strategies to address the challenge of harnessing the innate immune system in oxidative stress diseases of the neonate.
Keyphrases
- oxidative stress
- innate immune
- brain injury
- subarachnoid hemorrhage
- diabetic rats
- dna damage
- ischemia reperfusion injury
- induced apoptosis
- cerebral ischemia
- immune response
- signaling pathway
- public health
- endothelial cells
- multiple sclerosis
- heat shock
- white matter
- machine learning
- endoplasmic reticulum stress
- artificial intelligence
- heat shock protein