Acute Respiratory Distress Syndrome, or ARDS, is an often fatal complication of severe traumatic injury, bacterial infections, blood transfusions and overdoses of some medications. In ARDS, the lungs become swollen with fluid and breathing becomes impossible. Thirty percent to 40 percent of patients die. There is no effective treatment.
Sepsis, an overwhelming bacterial infection of the blood and organs, is the most common cause of ARDS. When the immune system responds to the infection, molecules called inflammatory cytokines and chemokines are released. These molecules attract inflammatory white blood cells and destroy bacteria, but also lead to fever, swelling and other symptoms of shock and can wreak havoc on the patient in the course of fighting off the infection.
"Without an inflammatory response, bacterial invaders in the lungs can kill, but too intense a response can also be fatal," said Kurt Bachmaier, University of Illinois at Chicago (UIC) research assistant professor in pharmacology and first author of the study. The researchers created a mouse model that lacks the gene for a protein, called Cblb, which was known to play a crucial role in chronic inflammation and auto-immunity through regulation of T- and B-cells.
When sepsis was induced in mice with and without the Cblb gene, there was a marked difference in the level of the inflammatory response and survival. Mice lacking the Cblb gene were much less likely to survive than control mice.
The UIC researchers were able to show how Cblb regulates the immune response. They showed that in normal mice, a receptor found in lung tissue that induces the release of inflammatory cytokines and chemokines disappears from the cell surface after about an hour, ending the signalling of the immune response. In the Cblb-deficient mice the receptor stays on the surface, and the inflammatory response is not turned off.
MEDICA.de; Source: University of Illinois at Chicago