Critical Care · 2020 · 91 citations · 2 references
Life SciencesImmunologyPharmacologyImmunopathologyImmunotherapyInflammationAcute InflammationCytokine BiologyCytokine TherapyCytokine-based TherapyCytokine-mediated PathologyInflammatory SignalingCovid-19-associated Acute Respiratory Distress SyndromeCytokine AntagonismCytokine Storm SyndromeCytokine Targeted TherapyInflammatory Bowel Disease ImmunopathogenesisTumor Necrosis Factor Inhibitor TherapyTumor Necrosis Factor Receptor 1 SignalingTumor Necrosis Factor Therapy
The severe acute respiratory coronavirus 2 (SARS-CoV-2) pandemic has prompted search for therapeutics tackling both the pathogen and the overwhelming host response, on an unprecedented scale.In a minority of patients, the disease may cause frequently lethal complications from acute respiratory distress syndrome to multisystem organ failure presumably driven by a cytokine storm [1].Therefore, anti-cytokine therapies may be helpful to prevent tissue injury.However, these antiinflammatory drugs constitute double-edged swords; while they can prevent organ damage, they increase the risk of concomitant (super)infection.Recently, Neurath argued for a protective effect of tumor necrosis factor (TNF) inhibitors in severe COVID-19 [2].Specifically, TNF may aggravate lymphopenia through direct killing via TNF/TNFR1 signaling in T cells [3], and T cell dysfunction reflects an important yet underestimated target for immunomodulatory interventions [4].Thus, anti-TNF strategies may be an interesting option in severe COVID-19.This is supported by data from patients with inflammatory bowel disease (IBD) already on anti-TNF treatment.As of June 16, 2020, outcome data from 1511 IBD patients with COVID-19, among them, 433 patients on anti-TNF, are available from the SECURE-IBD registry [5].Of these, 16% were hospitalized but only three patients (0.7%) died.Compared to other anti-inflammatory drugs such
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