Friday, 11 October 2013

Linking endotoxin and septic shock


Researchers at the University of North Carolina School of Medicine have identified a sensor pathway inside cells. The research indicates that both exterior and interior sensors work together to detect the same component of bacterial cell membranes: lipopolysaccharide (LPS).

By showing how the immune system distinguishes between suspicious activity and real threats, the study could lead to new therapies for septic shock -- when the immune system overreacts to a bacterial infection to such an extent that it causes more harm than good.

The body responds to a bacterial infection by increasing blood vessel permeability near the area under attack, which allows immune system cells to leave the bloodstream and seek and destroy the bacteria. Fluid also leaks into the area surrounding the infection, causing characteristic swelling. This is beneficial in fighting infection, but when the infection gets out of hand and these immune response occur throughout the body, blood pressure plummets, overtaxing the heart and leading to organ failure and often death. This syndrome is known as septic shock. About half of the cases of septic shock are caused by bacteria that produce LPS, also known as endotoxin. In fact, much of what is known about endotoxic shock comes from studying animals injected with high doses of LPS.

For further details, refer to the following paper:

Jon A. Hagar, Daniel A. Powell, Youssef Aachoui, Robert K. Ernst, and Edward A. Miao. Cytoplasmic LPS Activates Caspase-11: Implications in TLR4-Independent Endotoxic Shock. Science, 13 September 2013: 1250-1253 DOI: 10.1126/science.1240988

Posted by Tim Sandle