Critical Care Researchers Find Clues To Combat Sepsis

The research was published in the American Journal of Respiratory Critical Care Medicine.

“Sepsis can be considered as collateral damage from our own defense system,” says Dr. Mark Wewers, a pulmonologist and critical care specialist at Ohio State University Medical Center and principal investigator of the study. “We were able to show that caspase-1 contributes to this damage since its deletion has proven to protect organs from developing sepsis.”

The findings also showed that B lymphocytes, cells that make antibodies fight infectious organisms, die during sepsis. During sepsis, if caspase-1 was eliminated, B lymphocytes were not lost.

“Learning how to prevent the loss of B lymphocytes, perhaps by inhibiting caspase-1, may assist us in providing treatment options while allowing for the generation of antibodies to fight infection,” said Wewers. “We may be able, in the future, to develop drugs that can inhibit caspase-1 and potentially lessen the damage that occurs in response to sepsis.”

The data from the study provided strong support for the role of apoptosis, or programmed cell death, as a critical component of the sepsis connection to caspase-1. Under normal circumstances, the enzyme kills damaged cells to protect the body. But this study suggests that in sepsis, caspase-1 triggers death in cells the body needs to fight the infection. The prevention of apoptosis is considered a key to improving survival and decreasing mortality.

Along with Wewers, other Ohio State researchers involved in the study were Matthew Exline, NaTosha Gatson, Mark W. Hall, Judy Hart, Nina Knatz and Anasuya Sarkar.

Grants from the National Institutes of Health supported this research.