In the millions of tiny air sacs tasked with absorbing oxygen in Brett Breslow's lungs, the scene was chaos.
Some of the sacs were swollen with fluid that had leaked from surrounding blood vessels. Others had simply collapsed. The grim result: the Cherry Hill man was starved of oxygen, leading doctors at Cooper University Hospital to put him on a ventilator for 19 days.
Breslow was suffering from a massive bout of inflammation -- a catch-all description for the damage in many of the sickest patients with COVID-19. In addition to the assault on his lungs, the disease was harming his liver and kidneys, as well as causing him to form abnormal blood clots.
"It really attacked every organ in the body," said his wife, Amy.
Physicians have known for decades how to treat inflammation. In 1950, the Nobel Prize was given to researchers who found that in people with rheumatoid arthritis, inflammation could be calmed with steroids (not the kind used illegally by some athletes, but synthetic versions of a different class of hormones). Later that year, steroids were used to treat asthma, another widespread inflammatory condition.
And in June, researchers reported that dexamethasone, an inexpensive, generic steroid, improved the odds of survival for COVID-19 patients on ventilators.
But steroids are a brute-force approach. Though inflammation can be harmful, it also is one way the immune system fights off disease. From the start of the pandemic, physicians warned that if steroids were used to tamp down the collateral damage from inflammation, patients might be less able to fight off the initial cause of the problem: the coronavirus.
"They are like shotguns," Anita McElroy, a University of Pittsburgh infectious-disease specialist, said of the drugs. "They dampen all the immune response."
A new pair of studies from the University of Pennsylvania may offer a roadmap to a more targeted response. Researchers took blood samples from dozens of COVID patients and ran them through a boxy device called a flow cytometer, using laser beams to identify which kinds of immune cells had been activated to fight the disease.
The authors measured each patient's B-cells, which, if properly activated, make antibodies to fight the virus. They also measured various kinds of T-cells, including "helper" cells that play a role in marshaling the body's defenses, and "killer" cells, which destroy infected cells before the virus inside them spreads further. All cells were further categorized by molecular signatures that indicated their readiness to fight disease.