Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide. Even when patients survive the initial insult, there is significant morbidity and mortality secondary to subsequent pulmonary edema, acute lung injury and nosocomial pneumonia. While the relationship between TBI and secondary pulmonary complications is recognized, little is known about the mechanistic interplay of the two phenomena. Changes in mental status secondary to acute brain injury certainly impair airway- and lung-protective mechanisms. However, clinical and translational evidence suggest that more specific neuronal and cellular mechanisms contribute to impaired systemic and lung immunity that increases the risk of TBI-mediated lung injury and infection. To better understand the cellular mechanisms of that immune impairment, we review here the current clinical data that support TBI-induced impairment of systemic and lung immunity. Furthermore, we also review the animal models that attempt to reproduce human TBI. Additionally, we examine the possible role of damage-associated molecular patterns, the chlolinergic anti-inflammatory pathway and sex dimorphism in post-TBI acute lung injury. In the last part of the review, we discuss current treatments and future pharmacologic therapies, including fever control, tracheostomy and corticosteroids, aimed to prevent and treat pulmonary edema, acute lung injury and nosocomial pneumonia after TBI.
- intracranial pressure
- damage-associated molecular patterns
- pulmonary edema
- sex dimorphism
- Copyright © 2016, American Journal of Physiology-Lung Cellular and Molecular Physiology