CXCL8 is significantly upregulated in peripheral blood mononuclear cells of CAD patients and demonstrates good diagnostic discrimination (AUC 0.81), arguing for its potential utility as an inflammatory marker derived from PBMCs.
CXCL8 expression was significantly increased in PBMCs of CAD patients compared to healthy controls.
IRAK1, TRAF6, and MAPK1 showed increased expression in CAD patients but these differences were not statistically significant.
ROC curve analysis demonstrated that CXCL8 had good discriminative ability between CAD patients and healthy controls.
In multivariable binary logistic regression, only CXCL8 showed an independent relationship with CAD.
Protein-protein interaction network analysis indicated that IRAK1, TRAF6, and MAPK1 form an integrated upstream signalling module, while CXCL8 acts as a downstream inflammatory mediator.
The study used a case-control design with angiographically confirmed CAD diagnosis.
This research suggests that a specific immune signaling molecule called CXCL8 (also known as interleukin-8) is notably elevated in the blood immune cells of people with coronary artery disease (CAD) compared to healthy individuals. The study examined blood samples from 125 CAD patients confirmed by coronary angiography and 125 healthy controls, measuring the activity of four genes involved in inflammatory signaling pathways. While three genes (IRAK1, TRAF6, and MAPK1) showed a trend toward higher activity in CAD patients, only CXCL8 was significantly and independently associated with CAD. The researchers also assessed how well CXCL8 levels could distinguish between CAD patients and healthy controls. The analysis showed a relatively strong discriminative ability, with an area under the curve (AUC) of 0.81 — a statistical measure where values closer to 1.0 indicate better ability to tell two groups apart. This suggests CXCL8 measured from peripheral blood immune cells could potentially serve as a marker of CAD-related inflammation. Network analysis further showed that IRAK1, TRAF6, and MAPK1 likely work together as an upstream signaling group that could drive CXCL8 production, providing a biological explanation for why CXCL8 is elevated. This research suggests that measuring CXCL8 in circulating blood immune cells may offer a window into the chronic inflammation underlying coronary artery disease. However, as a case-control study, it cannot establish causation, and further research would be needed to determine whether CXCL8 levels change as disease progresses or in response to treatment, and whether it adds value beyond existing clinical tests.
Subramanian V, Kumar M, Muralidharan T, Venkatesan V. (2026). Peripheral immune cell expression of IRAK1, TRAF6, MAPK1 and CXCL8 in coronary artery disease.. Molecular biology reports. https://doi.org/10.1007/s11033-026-12710-0