Table 2.
Anti-inflammatory properties of immunomodulatory drugs
| Type of therapeutic | Drug(s) | Immunomodulatory effect(s) (reference[s]) |
|---|---|---|
| COX inhibitors | Mesalamine, celecoxib | Coadministration of COX inhibitors with zanamivir diminished cellular infiltrate and improved survival of H5N1 virus-infected mice compared to antiviral treatment alone (22, 157) |
| CCR2 inhibitor | PF-04178903 | Increased survival of mice infected with influenza virus and reduced lung immunopathology (87, 88) |
| Sphingosine receptor agonists | Suppresses cytokine and chemokine production; sphingosine receptors have been shown to play an important role in innate immune responses (120) | |
| Anti-TNF agents | Mediator of pulmonary inflammation during influenza A viral pneumonia; decreased severity of pulmonary immunopathology and prolonged survival of A/PR/8-infected mice (67) | |
| Statins | Simvastatin | Statins were not found to reduce the risk of developing severe disease in patients with pandemic influenza (H1N1) 2009 (144) |
| OX40 | OX40-Ig fusion proteins | OX40 plays a critical role in T-cell-mediated immunopathology in the lung during viral infection (65); ligation on activated T cells reduces pulmonary eosinophilia during Cryptococcus neoformans infection (64) |
| PPARα/PPARγ agonists | Gemfibrozil, pioglitazone, rosiglitazone, 15d-PGJ2, ciglitazone, troglitazone | 15d-PGJ2, ciglitazone, and troglitazone decreased production of IL-1α, IL-6, and TNF cytokines, CXCL8 and CCL5 chemokines, and ICAM-1 in RSV-infected lung epithelial cells (4); administration of gemfibrozil (intraperitoneally) on days 4 to 10 after exposure to H2N2 influenza virus and following the onset of illness significantly increased survival in mice with severe influenza (20) |