Stephen Galli, MD, the Mary Hewitt Loveless, MD, Professor and chair of pathology, and his colleagues have shown for the first time that mast cells can provide protection from a potentially deadly condition known as sepsis by destroying a molecule that contributes to the pathology and death associated with this bacterial infection. Their results are to be published in the Nov. 14 advance online edition of Nature. The first authors, Marcus Maurer, MD, and Jochen Wedemeyer, MD, were postdoctoral fellows in Galli's laboratory during the study.
"What we have uncovered in this study is a new role for the mast cell, which is to limit the amount of damage caused by endothelin-1, a molecule that is produced in high amounts by the body during severe sepsis, as well as in association with other disorders," said Galli.
Sepsis is a severe illness caused by overwhelming infection of toxin-producing bacteria in the bloodstream. The effects of sepsis in humans include a high fever, hyperventilation and diarrhea and can be life threatening, especially in patients with other medical problems.
During some infections, endothelin-1 levels can go very high, causing extreme dilation of the veins and contributing to some of the severe symptoms of sepsis. At the start of the study, the scientists already knew that, in cell culture, mast cells are activated by endothelin-1. In turn, the mast cells also can produce endothelin-1 and break it down. "However, it was not possible to guess what the net effect of the mast cells on the endothelin system would be, because mast cells can both
Contact: Mitzi Baker
Stanford University Medical Center