Clinical Potential of Immunotherapies in Subarachnoid Hemorrhage Treatment: Mechanistic Dissection of Innate and Adaptive Immune Responses

Abstract

Subarachnoid hemorrhage (SAH), classified as a medical emergency, is a devastating and severe subtype of stroke. SAH induces an immune response, which further triggers brain injury; however, the underlying mechanisms need to be further elucidated. The current research is predominantly focused on the production of specific subtypes of immune cells, especially innate immune cells, post-SAH onset. Increasing evidence suggests the critical role of immune responses in SAH pathophysiology; however, studies on the role and clinical significance of adaptive immunity post-SAH are limited. In this present study, we briefly review the mechanistic dissection of innate and adaptive immune responses post-SAH. Additionally, we summarized the experimental studies and clinical trials of immunotherapies for SAH treatment, which may form the basis for the development of improved therapeutic approaches for the clinical management of SAH in the future.

Transcriptomics and metabolomics reveal hypothalamic metabolic characteristics and key genes after subarachnoid hemorrhage in rats

“…In addition, changes in immune-related signaling (complement and coagulation cascades) were found in our study. The innate immune system was acutely activated after SAH, and the complement system was a major component of humoral immunity and a bridge linking innate and adaptive immunity during acute SAH (Zhang et al 2023 ). Complement activation may induce excessive synaptic pruning by SAH (complement components C1q and C3 are involved in synaptic removal) and cause brain damage (Van Dijk et al 2020 ).…”

The effect of transcutaneous auricular vagus nerve stimulation on cardiovascular function in subarachnoid hemorrhage patients: a safety study

“…Subarachnoid hemorrhage (SAH) is a devastating subtype of stroke that represents a significant global health burden and causes permanent disability in approximately 30% of survivors. 1,6,40 Early brain injury can occur within the first 24 to 48 hours after ictus, which involves a cascade of elevated intracranial pressure and a subsequent drop of cerebral perfusion. 4 Systemic and local inflammation, cerebral edema, blood-brain barrier (BBB) disruption, sympathetic nervous system activation, autoregulatory failure, microthrombosis, spreading depolarizations (SDs), and inflammation have all been observed during this period.…”