Drugs that control host cell pathways, including inflammation, tumor necrosis factor, interferons, and autophagy, can reduce the "cytokine storm" response to injury, control infection, and aid in cancer therapy.
Sevoflurane administration ameliorated a cytokine storm by decreasing serum levels of interleukin (IL)-1 and -6 and tumor necrosis factor (TNF)-α, and improved liver function was determined.
Upon intravenous injection of tumour necrosis factor (TNF) in mice, a systemic inflammatory response syndrome (SIRS) is initiated, characterized by an acute cytokine storm and induction of vascular hyperpermeability.
Immune challenge of invading macrophages at sites of infection is associated with release of TNF, which triggers a local cytokine storm as part of the normal inflammatory response.
Bacterial infection causes a pronounced macrophage (MΦ) and dendritic cell activation that leads to excessive pro-inflammatory cytokine IL-1β, IL-6 and TNF-α production (cytokine storm), resulting in endotoxic shock.
Cytokines were measured in cell-free supernatants at 2 h, and specific mRNA for tumour necrosis factor (TNF)-α, thought to be the initiator of the cytokine storm, was also measured in cell lysates by reverse transcription-polymerase chain reaction (RT-PCR).
These pathogenic T cells initiated a cytokine storm characterized by high levels of tumor necrosis factor (TNF) and interleukin 6 (IL-6), and depletion of T cells or blockade of these inflammatory cytokines prevented the lethal disease.