Sepsis, a life-threatening immune response to infection, can lead to tissue damage, organ failure and amputation; its mortality rate is 15 to 34 percent, and it is the most expensive condition treated in U.S. hospitals, accounting for 13 percent of hospital costs and an estimated $62 billion annually.
Early detection is a major challenge in managing sepsis, largely because it is heterogeneous and symptoms are often vague and may not be obvious. But now, researchers at Massachusetts General Hospital (MGH), Brigham and Women’s Hospital, the Massachusetts Institute of Technology (MIT), and the Broad Institute of MIT and Harvard have come a step closer to early diagnosis of sepsis and perhaps to the development of treatments that can stop it before it even begins. The findings are described in the journal Nature Medicine.
“The underlying problem is an abnormal immune response,” said corresponding co-author Marcia B. Goldberg, MD, a physician and researcher in MGH’s Infectious Diseases Division, a member of the Broad Institute, and a professor at Harvard Medical School. To tease out the cause, she and her colleagues — a multidisciplinary team of immunologists, infectious disease doctors, and engineers, all affiliated with Broad — looked at a small sample of hospitalized patients in early sepsis and a control group who had infections without sepsis. “We identified a new subset of monocytes, or innate immune cells, that was markedly expanded in the patients with sepsis.”
