The term “cytokine storm” (CS) refers to a spectrum of different immune dysregulation disorders characterized by constitutional symptoms, systemic inflammation and multiorgan dysfunction
[2][1]. The trigger for the CS is an uncontrolled immune response with the continuous activation and expansion of immune cells, lymphocytes and macrophages, which produce immense amounts of proinflammatory cytokines
[3][2]. In viral infections, the release of proinflammatory factors leads to apoptosis of lung epithelial cells, and pulmonary alveolar and microvascular endothelial cells, leading to complications such as alveolar edema and hypoxia. The uncontrolled production of proinflammatory factors, containing IL-6, IL-8, IL-1β and GM-CSF, and chemokines such as CCL2, CCL-5, IP-10 and CCL3, along with reactive oxygen species, results in pulmonary fibrosis
[4][3]. CXCL8 chemokine is also involved in the inflammation and trafficking of immune cells in the context of viral infections, as it has a chemotactic action for neutrophils and monocytes in the respiratory tract
[5][4]. The clinical picture of the cytokine storm, although variable, generally manifests itself as laboratory “overlap syndrome” with a decreased cell count, a decreased ESR, an increased ferritin level, NK dysfunction and hemophagocytosis
[6][5]. This clinically results in the increased perivascular infiltration of activated macrophages, neutrophils and fibroblasts, accompanied by extensive fibrin deposition and alveolar collapse, leading to acute respiratory distress syndrome (ARDS)
[7,8][6][7].