At least in bacterial sepsis, the non-redundant final common pathway of eGC damage appears to be the cleavage of heparan sulfate (HS) from glycosaminoglycans by the enzyme heparanase (HPSE) (28, 29), which is released mainly from endothelial cells by pro-inflammatory cytokines such as TNF-α, IL-1β and IL-6 (14, 30, 31). Here, IL6 is linked to bacterial infectious disease with sepsis.