Complex interactions exist between cytokines, and the interleukin family plays a fundamental role
in inflammation. Particularly circulating IL-1β, IL-6 and IL-8 are unregulated in systemic and chronic
inflammatory conditions. Hypercoagulability is an important hallmark of inflammation, and these cytokines
are critically involved in abnormal clot formation, erythrocyte pathology and platelet hyper-activation, and
these three cytokines have known receptors on platelets. Although these cytokines are always unregulated
in inflammation, we do not know how the individual cytokines act upon the structure of erythrocytes and
platelets, and which of the viscoelastic clot parameters are changed. Here we study the effects of IL-1β,
IL-6 and IL-8 at low physiological levels, representative of chronic inflammation, by using scanning electron
microscopy and thromboelastography. All three interleukins caused the viscoelastic properties to display
an increased hypercoagulability of whole blood and pathology of both erythrocytes and platelets. The most
pronounced changes were noted where all three cytokines caused platelet hyper-activation and spreading.
Erythrocyte structure was notably affected in the presence of IL-8, where the morphological changes
resembled that typically seen in eryptosis (programmed cell death). We suggest that erythrocytes and
platelets are particularly sensitive to cytokine presence, and that they are excellent health indicators.