FEATURES OF AUTOIMMUNITY IN THE ABDOMINAL AORTIC-ANEURYSM

Citation
Ak. Gregory et al., FEATURES OF AUTOIMMUNITY IN THE ABDOMINAL AORTIC-ANEURYSM, Archives of surgery, 131(1), 1996, pp. 85-88
Citations number
16
Categorie Soggetti
Surgery
Journal title
ISSN journal
00040010
Volume
131
Issue
1
Year of publication
1996
Pages
85 - 88
Database
ISI
SICI code
0004-0010(1996)131:1<85:FOAITA>2.0.ZU;2-#
Abstract
Purpose: Previous work has revealed that nonspecific abdominal aortic aneurysms (AAAs) have a prominent infiltration of inflammatory cells a nd that soluble extracts of AAA tissue are rich in immunoglobulins. Th ese observations raise the question whether autoimmune mechanisms play a role in the pathogenesis or progression of AAA disease. The hypothe sis of this investigation was that IgG purified from aneurysmal specim ens would be immunoreactive with normal components of the aortic wall (by means of immunohistochemistry) and with soluble proteins extracted from normal aortic tissue (by Western immunoblotting methods). Method s: Immunoglobulin G extracted from AAA homogenates was used to detect immunohistochemical reactivity to connective tissue components in fixe d sections of normal aorta obtained from an organ donor. Immunoblottin g techniques were used to compare the reactivity of IgG (detected with secondary goat antihuman antibody) from 14 patients with AAA with sol uble proteins extracted from normal and aneurysmal aortas. Immunoglobu lins G purified from extracts obtained from nine patients with no AAA were used for control experiments. Results: A unique band at approxima te to 80 kd was visualized when the filters were probed with IgG from 11 (79%) of 14 patients with AAA compared with only one (11%) of nine control subjects (P=.002 by Fisher's exact test). Immunoglobulins G fr om patients with AAA codistributed with matrix fibers in normal aortic sections, particularly in the adventitia (suggestive of a microfibril lar component). Conclusion: Our findings suggest that there are autoim mune features of AAA disease that might not only be informative in ter ms of AAA origin but also lead to more precise forms of pharmacologic down-regulation of disease progression.