Targeting inflammation in hypertension

Hypertension remains a global health and socioeconomic burden. Immune mechanisms are now recognized as integral part of the multifactorial etiology of hypertension and related organ damage. The present review addresses inflammatory pathways and immune targets in hypertension, which may be important for an immunomodulatory treatment of hypertension aside from lowering arterial pressure. RECENT FINDINGS: Anti-inflammatory interventions targeting single interleukins or almost the entire immune system show different beneficial effects. While immunomodulation (targeting specific portion of immune system) shows beneficial outcomes in certain groups of hypertensives, this does not pertain to immunosuppression (targeting entire immune system). Immunomodulatory interventions improve outcomes of hypertension independent of arterial pressure. The studies reveal interleukins, such as interleukin (IL)-1β and IL-17 as targets of immunomodulation. Besides interleukins, targeting αvβ-3 integrin and matrix metalloproteinase-2 or using experimental cell-therapy demonstrate beneficial effects in hypertensive organ damage. The NLR family pyrin domain containing 3 (NLRP3) inflammasome/IL-1β/endothelial cell/T-cell axis seems to be an important mediator in sustained inflammation during hypertension. SUMMARY: Although immunomodulation may be advantageous as a causal therapy in hypertension, targeting immune networks rather than single interleukins appears of major importance. Further research is required to better identify these networks and their links to human hypertension.