Immunomodulation is a general term for any process that changes the state of the immune system. Statins are cholesterol-reducing medications that have become a cornerstone of primary and secondary prevention of cardiovascular disease. In recent years, pleiotropic effects of statins have been highlighted including immunomodulatory properties in conditions as diverse as rheumatoid arthritis and COPD. Statins exert these effects on the inflammatory responses in part through modulating lymphocyte adhesion to endothelial cells. Experimental evidence in animals has indicated that statins may prevent sepsis and modulate its severity. Sepsis continues to be an increasingly frequent and acute medical problem in critically ill patients in the intensive care unit.

The mechanisms through which statins influence sepsis associated inflammation are currently poorly understood. However, it is proposed that statins inhibit the expansion of αβ T-cells to γδ T-cells. In sepsis patients the γδ T-cell population is predominant (sepsis model). Statins are also proposed to inhibit the binding of γδ T-cells to ICAM-1 on endothelial cells (sepsis/statin model). Using the Cellix Microfluidic SP1.0 Platform, the adhesion profile of statin treated αβ T-cells from a mixed-sepsis model subjected to physiological shear stresses was assessed to determine the role played by T-cell LFA-1–ICAM binding.