CXCL8 upregulation mediates inflammatory cell infiltration and accelerates abdominal aortic aneurysm progression
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Published on: September 28, 2015
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.
