In a new study, researchers found that a cytokine ‘hurricane’ centered in the lungs drives respiratory symptoms in patients with severe COVID-19.
The research was conducted by a team at Columbia University.
Numerous COVID studies have focused on identifying immune responses in blood; a few have looked at airway samples from a single time point or from autopsies.
In the study, the team collected respiratory immune cells from 15 COVID-19 patients who had been intubated.
Each patient spent four to seven days on a ventilator, and airway and blood samples were obtained daily.
found two cytokines, CCL2 and CCL3, appear critical in luring immune cells, called monocytes, from the bloodstream into the lungs, where the cells launch an overaggressive attempt to clear the virus.
Targeting these specific cytokines with inhibitors may calm the immune reaction and prevent lung tissue damage.
Currently, one drug that blocks immune responses to CCL2 is being studied in clinical trials of patients with severe COVID-19.
The team found that survivors of severe COVID-19 had a greater abundance of antiviral T cells in their lungs than patients who died.
In patients with severe COVID-19, the lungs are damaged, and patients need supplemental oxygen. The risk of mortality is over 40%.
This suggests that these T cells may be critical in helping patients control the virus and preventing a runaway immune response.
The findings also may explain why trials of other cytokine inhibitors, including tocilizumab, have shown variable efficacy.
Tocilizumab inhibits the cytokine IL-6, which is elevated in patients with severe COVID but does not appear to be a major component of inflammation in the lung.
The study is one of the first to examine the immune response as it unfolds in real-time inside the lungs and the bloodstream in patients who are hospitalized with severe COVID-19.
One author of the study is Donna Farber, Ph.D. The study is published in the journal Immunity.
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