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Published on: September 28, 2015
CXCL8 upregulation mediates inflammatory cell infiltration and accelerates abdominal aortic aneurysm progression
Yulong Huang1, Xinsheng Xie1, Guoqiang Huang2
1Department of Vascular Surgery, Xiamen Branch of Zhongshan Hospital, Fudan University, Xiamen, China.
Objective:
To explore abdominal aortic aneurysm (AAA) pathogenesis and identify early diagnostic markers, providing a theoretical basis for novel preventive and therapeutic strategies.
Methods:
Gene expression profiles were retrieved from the Gene Expression Omnibus database (datasets: GSE7084, GSE47472, and GSE57691) comprising messenger RNA data from the aortic samples of 69 patients with AAA and 25 non-AAA controls. Data were merged and normalized; bioinformatics analysis was conducted on upregulated differentially expressed genes.
Results:
C-X-C motif chemokine ligand 8 (CXCL8) was prominently involved in regulating the chemokine signaling pathway. CXCL8 expression was significantly higher in the aortic walls of patients with AAA than that of controls. NLRP3, interleukin (IL)-18, and IL-1β expression levels were upregulated in patients with AAA and positively correlated with CXCL8 expression. CXCL8 may directly or indirectly interact with NLRP3.
Conclusions:
CXCL8 was upregulated in patients with AAA and induced inflammatory cell infiltration and cytokine secretion. CXCL8-induced NLRP3 inflammasome regulation triggered pyroptosis in vascular smooth muscle cells, exacerbating inflammation and tissue damage in the aortic wall. This degeneration of the aortic media accelerated AAA progression.
