Macrophage imbalance (M1 vs. M2) and upregulation of mast cells in wall of ruptured human cerebral aneurysms: preliminary results

Document Type

Article

Abstract

BACKGROUND: M1 and M2 cells are two major subsets of human macrophages that exert opposite effects on the inflammatory response. This study aims to investigate the role of macrophage M1/M2 imbalance and mast cells in the progression of human cerebral aneurysms to rupture. METHODS: Ten patients with cerebral aneurysms (five ruptured and five unruptured) underwent microsurgical clipping. During the procedure, a segment of the aneurysm dome was resected and immunostained with monoclonal antibodies for M1 cells (anti-HLA DR), M2 cells (anti-CD 163), and mast cells (anti-tryptase clone AA). A segment of the superficial temporal artery (STA) was also removed and immunostained with monoclonal antibodies for M1, M2, and mast cells. RESULTS: All ten aneurysm tissues stained positive for M1, M2, and mast cells. M1 and M2 cells were present in equal proportions in unruptured aneurysms. This contrasted with a marked predominance of M1 over M2 cells in ruptured aneurysms (p = 0.045). Mast cells were also prominently upregulated in ruptured aneurysms (p = 0.001). Few M1 and M2 cells were present in STA samples. CONCLUSIONS: M1/M2 macrophages and mast cells are found in human cerebral aneurysms; however, M1 and mast cell expression seems to markedly increase in ruptured aneurysms. These findings suggest that macrophage M1/M2 imbalance and upregulation of mast cells may have a role in the progression of cerebral aneurysms to rupture.

Medical Subject Headings

Adult; Aged; Aneurysm, Ruptured (complications, pathology); Antigens, CD (metabolism); Antigens, Differentiation, Myelomonocytic (metabolism); Female; HLA-DR Antigens (metabolism); Humans; Intracranial Aneurysm (complications, pathology); Macrophages (metabolism); Male; Mast Cells (classification, metabolism, pathology); Middle Aged; Receptors, Cell Surface (metabolism); Temporal Arteries (pathology); Up-Regulation (physiology)

Publication Date

9-21-2012

Publication Title

Journal of neuroinflammation

E-ISSN

1742-2094

Volume

9

First Page

222

PubMed ID

22999528

Digital Object Identifier (DOI)

10.1186/1742-2094-9-222

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