Cayman's Lipidomics Services team use their targeted eicosanoid and oxylipin panels to help researchers at the University of Rochester detect biomarkers of inflammation in COVID-19.

Smoking has been added to the risk factors related to poorer outcomes of SARS-CoV-2 infection, with reports that COVID-19 is likely to be more severe in these patients. Investigators in a preprint available through medRxiv have associated a distinct profile of inflammatory markers that mediate viral-host interactions with COVID-19 pathogenesis and demonstrate that many of these markers are higher in smokers with COVID-19. Here are the main findings:

• Pro-inflammatory cytokine (e.g., IL-1α, IL-8, IL-2, VEGF, IL-10) levels are higher in patients with COVID-19 compared to COVID-19-negative controls. In COVID-19 patients with a history of smoking, there is a significant release of hyperinflammatory cytokines (e.g., IFN-γ, eotaxin, MCP-1, IL-9) compared to non-smokers.

• Angiotensin-converting enzyme 2 (ACE2), which mediates entry of SARS-CoV-2 into host cells, is also increased in COVID-19 patients compared to controls, even more so in COVID-19 patients with a history of smoking.
  

• Furin, the enzyme needed to prime the spike protein of SARS-CoV-2 for fusion with host cells, is also higher in COVID-19 patients with a history of smoking, compared to non-smokers with COVID-19.

• The lipid mediators prostaglandin F_2α, leukotriene B₄, lipoxin A₄, 5-hydroxyeicosatetraenoic acid (HETE), and 20-HETE are increased in COVID-19 patients compared to those who recovered from the infection. Smoking, however, does not appear to be linked to changes in these lipid pathways

This work is an important step in developing these inflammatory and lipid mediators as biomarkers to indicate disease severity in COVID-19 patients, which would help to provide more effective care for recovery.

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