Journal of clinical pathology · 1994
Cytokine gene expression in aortic adventitial inflammation associated with advanced atherosclerosis (chronic periaortitis).
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Ramshaw A L, Roskell D E, Parums D V
Аннотация
AIMS: To determine whether aortic adventitial chronic inflammation associated with advanced atherosclerosis ("chronic periaortitis") is associated with any detectable cytokine gene expression.
METHODS: RNA was extracted from six fresh surgical specimens of atherosclertic aortic aneurysm wall showing a spectrum of chronic periaortitis. Controls included four normal aortas and an HUT 78 T cell line. Reverse transcriptase and the polymerase chain reaction (PCR) were used to amplify mRNA for interleukins-1 alpha (IL-1 alpha), -2 (IL-2), -4 (IL-4), IL-2 receptor-alpha (IL-2R-alpha), tumour necrosis factor alpha (TNF-alpha) and gamma interferon (IFN-gamma) with beta-actin as an internal control.
RESULTS: No TNF-alpha mRNA was detected in any of the inflamed aortic tissue samples, in contrast to the aortic T lymphocytes propagated in culture in IL-2 conditioned medium (aortic cultured T cells) and peripheral blood mononuclear cells from these patients. In contrast, IFN-gamma, IL-1 alpha, IL-2, IL-2 receptor and IL-4 PCR products were detected for each inflamed aortic tissue RNA sample with IFN-gamma mRNA expression increasing with increasing degrees of adventitial inflammation. Only beta-actin mRNA was present in the normal aorta.
CONCLUSIONS: These findings indicate the active nature of aortic adventitial chronic inflammation associated with human advanced atherosclerosis ("chronic periaortitis") and show its possible progressive potential to the clinically important diseases termed "idiopathic retroperitoneal fibrosis" and "inflammatory aneurysm".
METHODS: RNA was extracted from six fresh surgical specimens of atherosclertic aortic aneurysm wall showing a spectrum of chronic periaortitis. Controls included four normal aortas and an HUT 78 T cell line. Reverse transcriptase and the polymerase chain reaction (PCR) were used to amplify mRNA for interleukins-1 alpha (IL-1 alpha), -2 (IL-2), -4 (IL-4), IL-2 receptor-alpha (IL-2R-alpha), tumour necrosis factor alpha (TNF-alpha) and gamma interferon (IFN-gamma) with beta-actin as an internal control.
RESULTS: No TNF-alpha mRNA was detected in any of the inflamed aortic tissue samples, in contrast to the aortic T lymphocytes propagated in culture in IL-2 conditioned medium (aortic cultured T cells) and peripheral blood mononuclear cells from these patients. In contrast, IFN-gamma, IL-1 alpha, IL-2, IL-2 receptor and IL-4 PCR products were detected for each inflamed aortic tissue RNA sample with IFN-gamma mRNA expression increasing with increasing degrees of adventitial inflammation. Only beta-actin mRNA was present in the normal aorta.
CONCLUSIONS: These findings indicate the active nature of aortic adventitial chronic inflammation associated with human advanced atherosclerosis ("chronic periaortitis") and show its possible progressive potential to the clinically important diseases termed "idiopathic retroperitoneal fibrosis" and "inflammatory aneurysm".