Cerebrospinal fluid proteomics reveals inflammatory activation in aneurysmal subarachnoid hemorrhage irrespective of HIV status.

OBJECTIVES

People with HIV (PWH) are at increased risk of cerebrovascular abnormalities, including aneurysmal subarachnoid hemorrhage (SAH). However, it is unclear whether HIV-associated inflammation contributes significantly to the inflammatory response observed in the cerebrospinal fluid (CSF) during aneurysm rupture. Here, we used high-throughput Olink proteomics to compare inflammatory marker profiles in CSF between participants with aneurysmal SAH and PWH without aneurysms.

DESIGN

This was a cross-sectional observational study which enrolled participants who were indicated for endovascular coil embolization due to ruptured anterior communicating artery aneurysms ( n  = 30) or who underwent clinically indicated lumbar puncture as part of the workup for nonneurovascular conditions ( n  = 9).

METHODS

We performed a lumbar puncture and analyzed CSF samples from individuals presenting with aneurysmal SAH ( n  = 30) and PWH without any known vascular disorder ( n  = 9). Among the aneurysm patients, 13 were PWH and 17 were HIV-negative. An Olink Target 96 Inflammation panel was used to quantify inflammatory proteins.

RESULTS

Among 68 detectable inflammatory proteins, 43 were significantly upregulated in participants with aneurysms ( n  = 30) compared to PWH without aneurysm ( n  = 9). A similar inflammatory signature was observed in HIV-negative aneurysm participants ( n  = 17) and PWH with aneurysm ( n  = 13), with no significant differences between these two groups. Interleukin-6 (IL-6) was the most upregulated protein across all aneurysm to nonaneurysm comparisons. These findings suggest that aneurysm rupture is associated with a strong CSF inflammatory response, largely independent of HIV status.

CONCLUSION

Ruptured intracranial aneurysms are associated with strong upregulation of inflammatory proteins in the CSF. This inflammatory response appears independent of HIV infection.