Aneurysmal subarachnoid haemorrhage (aSAH), resulting from the rupture of intracranial aneurysms, can yield high mortality and disability. This study aimed to explore the immune infiltration of aneurysmal tissues and investigate a novel mechanism underlying aSAH. We downloaded datasets containing expression profiles of aneurysmal and normal arterial tissues from the online database. Then a comprehensive bioinformatic strategy was conducted to select the biomarkers of aneurysmal tissues.Two calculation algorithms were performed to identify the unique immune characteristics between aneurysmal tissues and normal arteries. Double immunofluorescence staining was used to investigate the role of pathway-related proteins in the inflammatory process after aSAH. Six microarray datasets were integrated, and another RNA-sequencing dataset was used as the validation dataset. Functional enrichment analysis of the differentially expressed genes indicated that immune-related processes were closely related to the progression of aSAH. We then performed immune microenvironment infiltration analysis, and the results suggested macrophages were abnormally enriched in aneurysmal tissues. Core gene MSR1 was filtered through a comprehensive bioinformatic strategy. Our analysis suggested that MSR1 might be associated with macrophage activation and migration. Our study elucidated the impact of macrophage and MSR1 on aSAH progression. These findings were helpful in gaining insight into the immune heterogeneity of aneurysmal tissues and normal arteries, and in identifying patients who might benefit from immunotherapy.
| INTRODUCTIONAneurysmal subarachnoid haemorrhage (aSAH) is a deadly cerebrovascular disease. [1][2][3] It is estimated that more than 25% of patients with aSAH died in the hospital, and more than 40% have persistent neurological deficits. 2 Moreover, patients who survive the initial haemorrhage are susceptible to cerebrovascular diseases and have mortality rates that exceed the general population. 3,4 For example, the recurrence of aSAH in survivors was estimated to be 15-times higher than that in the general population. Thus, it is critical to recognize the cellular and molecular differences between aneurysmal tissues from aSAH patients and normal intracranial arterial tissues, which could offer a theoretical basis for the high recurrence of cerebrovascular disease in patients with aSAH.Inflammatory reactions are involved in the formation, progression and deterioration of aSAH. 5 Once the intracranial aneurysm (IA) ruptures, immune cells, haemoglobin and cytokines enter the central nervous system and mediate inflammatory responses. 6,7 Xing Wang and Dingke Wen contributed equally to this work as first authors.