Anti-inflammatory effects of beta-blockers in new coronavirus infection (COVID-19)

The review article presents data from scientific studies on the anti-inflammatory possibilities of using beta-blockers (BB) in the new coronavirus infection (COVID-19). Preventing the disease from progressing into a hyper-inflammatory phase can give the body the time it needs to recover, because the damage is not caused by the virus itself, but by an excessive immune response to the virus. Thus, finding therapies to prevent or slow the progression of the disease to the point of developing a hyperinflammatory process and a cytokine storm will be of paramount importance. Activation of β2-adrenergic receptors leads to the formation of reactive oxygen species (ROS), which trigger the secretion of inflammatory cytokines. Moreover, catecholamines (β2-adrenergic receptor activators) may promote the development of inflammatory lymphocytes (especially the Th17 response), which have been recognized as being responsible for the severe immune response associated with COVID-19. β2-adrenergic receptors are expressed in the airways and on all immune cells such as macrophages, dendritic cells, B and T lymphocytes. Blocking β2-adrenergic receptors reduces the Th-17 response and suppresses the modulation of inflammatory cytokines, including IL-6, while increasing interferon-γ. Non-selective BBs are currently being used to treat several conditions and have been shown to reduce stress-induced inflammation and reduce anxiety. BBs do not prevent viral replication and spread, but on the other hand, the proposed beta-blocker strategy may help mitigate cytokine storm-induced inflammation in COVID-19 patients, thereby reducing mortality. The review article highlights the importance of targeting therapeutic interventions to β2-adrenergic receptors early in COVID-19, which may be beneficial in preventing the hyperinflammatory process.