Inflammation in Aneurysmal Subarachnoid Hemorrhage: Cause, Consequence, or Both? Focus on Pathogen Pattern Recognition

Abstract

Inflammation plays a key role in the formation, progression, and rupture of intracranial aneurysms, leading to aneurysmal subarachnoid hemorrhage. Pathogen PPRs (pattern recognition receptors) that are activated by pathogen-derived molecules are key mediators of the innate immune response against microbes. As PPRs are activated by molecules resembling microbes, that is, pathogen-associated molecular patterns or damage-associated molecular patterns that can be of nonmicrobial origin, exposure to pathogen-associated molecular patterns and damage-associated molecular patterns may promote an excessive inflammatory response, promoting excessive cell death and tissue remodeling. We present a narrative review describing the role of PPRs, pathogen-associated molecular patterns, and damage-associated molecular patterns in the formation, progression, and eventual rupture of intracranial aneurysms, as well as in the neuronal damage caused by aneurysmal subarachnoid hemorrhage. Furthermore, we discuss putative therapeutic approaches to prevent the death and disability caused by intracranial aneurysm rupture and subsequent aneurysmal subarachnoid hemorrhage.