Localized increase of chemokines in the lumen of human cerebral aneurysms.

Journal Article (Journal Article)

BACKGROUND AND PURPOSE: Inflammation may play an important role in the formation and rupture of cerebral aneurysms. Chemokines act as chemoattractants for leukocytes directing them toward sites of tissue inflammation. The purpose of this study was to determine whether chemokines and chemoattractant cytokines were increased in the lumen of human cerebral aneurysms. METHODS: The concentrations of chemokines and other inflammatory molecules in blood samples drawn from the lumen of human cerebral aneurysms of 16 consecutive patients (harboring 18 aneurysms) were compared with blood samples from the femoral arteries of the same patients. Three aneurysms had ruptured. RESULTS: The mean plasma concentration of regulated on activation, normal T cell expressed and secreted (RANTES), monokine-induced-by-γ-interferon (MIG), interferon-γ-induced protein-10 (IP-10), eotaxin, interleukin (IL) 8, and IL17 was significantly higher in samples taken from cerebral aneurysms compared with femoral arteries. In contrast, plasma concentrations of all remaining inflammatory molecules (except IL6) that were tested did not differ between cerebral aneurysms and femoral arteries. For unruptured aneurysms, there was a significantly higher mean plasma concentration of monocyte chemoattractant protein-1 as well as RANTES, MIG, IP-10, eotaxin, IL8, and IL17 in samples obtained from cerebral aneurysms. CONCLUSIONS: High plasma concentrations of chemokines (monocyte chemoattractant protein-1, RANTES, MIG, IP-10, and eotaxin) and chemoattractant cytokines (IL8 and IL17) were found in the lumen of human cerebral aneurysms. These findings suggest that there may be an active recruitment of inflammatory cells into the aneurysm wall that may be exploited therapeutically.

Full Text

Duke Authors

Cited Authors

  • Chalouhi, N; Points, L; Pierce, GL; Ballas, Z; Jabbour, P; Hasan, D

Published Date

  • September 2013

Published In

Volume / Issue

  • 44 / 9

Start / End Page

  • 2594 - 2597

PubMed ID

  • 23887838

Pubmed Central ID

  • PMC3829607

Electronic International Standard Serial Number (EISSN)

  • 1524-4628

Digital Object Identifier (DOI)

  • 10.1161/STROKEAHA.113.002361


  • eng

Conference Location

  • United States