Abstract
The incidence of traumatic brain injury (TBI) has increased over the last years with an important impact on public health. Many preclinical and clinical studies identified multiple and heterogeneous TBI-related pathophysiological mechanisms that are responsible for functional, cognitive, and behavioral alterations. Recent evidence has suggested that post-TBI neuroinflammation is responsible for several long-term clinical consequences, including hypopituitarism. This review aims to summarize current evidence on TBI-induced neuroinflammation and its potential role in determining hypothalamic-pituitary dysfunctions.
Highlights
Traumatic brain injury (TBI) is defined as the consequence of an external impact force, which is able to induce a transient or permanent damage of the structure and function of the central nervous system (CNS) [1,2]
The primary damage initiates a cascade of biochemical, metabolic, and inflammatory alterations leading to secondary injury, which is associated with glutamatergic excitotoxicity, vascular dysfunction, calcium overload, and neuroinflammation [4,5,6,7,8]
Serum against pituitary (APA) and against the hypothalamus (AHA) concentrations were detected in 22.9% and 21.3% of subjects, respectively, and were directly associated with the onset of pituitary dysfunctions, strengthening the hypothesis that autoimmunity could be involved in the onset of TBI-induced hypopituitarism [45]
Summary
Traumatic brain injury (TBI) is defined as the consequence of an external impact force, which is able to induce a transient or permanent damage of the structure and function of the central nervous system (CNS) [1,2]. Cellular membrane disruption associated with the primary mechanical injury causes the release of damage associated molecular patterns (DAMPs) such as DNA and RNA, high mobility group box 1 (HMGB1), S-100 proteins, adenosine triphosphate, uric acid, lysophospholipids, and lipid peroxidation-derived carbonyl adducts of proteins [61,62] Through their binding to the Pattern Recognition Receptors (PRRs) on myeloid and dendritic cells, these molecules initiate the complex cascade of mechanisms that lead to post-traumatic neuroinflammation [61,63,64]. Some evidence suggested that the presence of autoreactive T-cells is not necessarily associated with the development of pathological autoimmunity [88], and a T cell-dependent neuroprotective response after TBI has been documented in different models of CNS injury [89] This represents the so-called “protective autoimmunity”, which is mediated by the production of neurotropic factors from autoreactive lymphocytes that are capable of promoting the recovery of injured neurons [90,91]. TBI-related tight-junction alterations can modify the distal end-feet of tanycytes, that are known to regulate the secretion of hypothalamic neuropeptides [113], compromising the physiological functioning of the hypothalamus-pituitary axis
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