Rationales and uncertainties for aspirin use in COVID-19: a narrative review

Figure 1. COVID-19-induced inflammation, endotheliopathy and thrombosis. Alveolar-capillary endothelial cells can be activated by SARS-CoV-2 infection leading to cytokine release and expression of vascular adhesion molecules. Also, endothelial cells express ACE which allows infection by SARS-CoV-2. This could trigger endothelial dysfunction and pyroptosis that also increase the pro-inflammatory stimuli and thrombogenic events.12 This figure was used with permission from the publisher Wolters Kluwer Health (license number: 4938390247706). ‘The Creative Commons license does not apply to this content. Use of the material in any format is prohibited without written permission from the publisher, Wolters Kluwer Health. Please contact permissions@lww.com for further information’. ICAM-1, intercellular adhesion molecule 1; IL, interleukin; TNF, tumour necrosis factor.

Figure 2. Mechanisms in which aspirin can manipulate the process in sepsis and acute respiratory distress syndrome: aspirin inhibits the enzyme COX, preventing the formation of pro-inflammatory thromboxane and prostaglandins. It also inhibits the release of NFκB from its inhibitor IkB, preventing the formation of pro-inflammatory cytokines and chemokines. Aspirin leads to the production of aspirin-triggered lipoxin, which induces the release of NO, inhibits the production of IL-8 and MPO, restores neutrophil apoptosis and promotes resolution. Aspirin increases the production of NO, resulting in reduced migration and infiltration of neutrophils and reduced permeability of the endothelium. 15-epi-ATL, aspirin-triggered 15-epi-lipoxinA4; AA, arachidonic acid; COX, cyclooxygenase; eNO, endothelial nitric oxide; IKK, IkB kinase; IL-8, interleukin 8; MPO, myeloperoxidase; NFκB, nuclear factor kappa B; NO, nitric oxide; PGE 2, prostaglandin E2; TXA 2, thromboxane.35 This image is licensed under the Creative Commons Attribution 4.0 International License found at http://creativecommons.org/licenses/by/4.0/.