A group of 15 serum inflammatory biomarkers representing a variety of those putatively involved in the inflammatory cascade was grouped and assessed in a cross-sectional study involving 960 stroke-free subjects. The biomarker panel was grouped as follows: systemic inflammation (high-sensitivity C-reactive protein [hsCRP], interleukin-6, and tumor necrosis factor-α); endothelial-related inflammation (E-selectin, P-selectin, intercellular adhesion molecule 1, vascular cell adhesion molecule 1 [VCAM-1], CD40 ligand, lipoprotein-associated phospholipase A2, chitinase-3-like-1 protein, total homocysteine [tHCY]); and media-related inflammation (matrix metalloproteinases-2, -3, and -9, and osteopontin). The association(s) between different inflammatory groups and white matter hyperintensity (WMH), lacunes, cerebral microbleeds (CMBs), enlarged perivascular space (PVS), and the number of deep medullary veins (DMVs) were investigated.

High levels of serum endothelial-related inflammatory biomarkers were associated with both increased WMH volume (R²=0.435, p=0.015) and the presence of lacunes (R²=0.254, p=0.027). Backward stepwise elimination of individual inflammatory biomarkers for endothelial-related biomarkers revealed that VCAM-1 was significant for WMH (β=0.063, p=0.005) and tHCY was significant for lacunes (β=0.069, p<0.001). There was no association between any group of inflammatory biomarkers and CMBs or PVS. Systemic inflammatory biomarkers were associated with fewer DMVs (R²=0.032, p=0.006), and backward stepwise elimination of individual systemic-related inflammatory biomarkers revealed that hsCRP (β= -0.162, p=0.007) was significant.

WMH and lacunes were associated with endothelial-related inflammatory biomarkers, and fewer DMVs was associated with systemic inflammation, thus suggesting different underlying inflammatory processes and mechanisms.