OBJECTIVES: To investigate (i) elastin degradation and the possible association between proteolysis and inflammation in abdominal aortic aneurysm disease (AAA), and (ii) the presence of cytomegalovirus (CMV) infection in the walls of AAA. MATERIALS: Specimens from 12 infrarenal AAAs, eight aortas with occlusive disease (AOD) and two normal aortas were studied by conventional light microscopy, immunohistochemistry using a monoclonal anti-elastin antibody BA-4 and anti-CMV antibody and transmission electron microscopy (TEM). MAIN RESULTS: In AAA the decrease in elastin immunoreactivity and the presence of elastin degradation was associated with increased mononuclear inflammatory cell infiltrates (p = 0.004 and p = 0.00002, respectively). The CMV immunostainings of the normal aortic wall and all the AAA and AOD samples were negative, nor could any CMV particles be demonstrated by TEM. CONCLUSIONS: The chronic inflammation and degradation of elastin in AAA suggests a possible immune-mediated mechanism. The inflammation may be induced by the chemotactic properties of elastin-derived peptides.
OBJECTIVES: To investigate (i) elastin degradation and the possible association between proteolysis and inflammation in abdominal aortic aneurysm disease (AAA), and (ii) the presence of cytomegalovirus (CMV) infection in the walls of AAA. MATERIALS: Specimens from 12 infrarenal AAAs, eight aortas with occlusive disease (AOD) and two normal aortas were studied by conventional light microscopy, immunohistochemistry using a monoclonal anti-elastin antibody BA-4 and anti-CMV antibody and transmission electron microscopy (TEM). MAIN RESULTS: In AAA the decrease in elastin immunoreactivity and the presence of elastin degradation was associated with increased mononuclear inflammatory cell infiltrates (p = 0.004 and p = 0.00002, respectively). The CMV immunostainings of the normal aortic wall and all the AAA and AOD samples were negative, nor could any CMV particles be demonstrated by TEM. CONCLUSIONS: The chronic inflammation and degradation of elastin in AAA suggests a possible immune-mediated mechanism. The inflammation may be induced by the chemotactic properties of elastin-derived peptides.
Authors: Jiusong Sun; Galina K Sukhova; Jie Zhang; Han Chen; Sara Sjöberg; Peter Libby; Mingcan Xia; Na Xiong; Bruce D Gelb; Guo-Ping Shi Journal: Arterioscler Thromb Vasc Biol Date: 2011-08-04 Impact factor: 8.311
Authors: L S Ang; W A Boivin; S J Williams; H Zhao; T Abraham; K Carmine-Simmen; B M McManus; R C Bleackley; D J Granville Journal: Cell Death Dis Date: 2011-09-08 Impact factor: 8.469