Scientists discover how plague avoids inflammatory response

A recently published study explains how the plague-causing bacteria Yersinia pestis evades detection and destruction by the human body's immune system.

Under most circumstances, certain immune cells will self-destruct if they are invaded or detect the presence of a pathogen. The process, called pyroptosis, eliminates a critical location for the germs to replicate. In addition, when the cells splits open, they release a series of chemical signals alerting the body of an attack, according to

The signals also reveal the infection's location. As more and more immune cells arrive to fight the infection, tissues become inflamed. By avoiding the pyroptic response, Y. pestis can avoid the resulting inflammation.

The authors of the study, which was led by Dr. Christopher LaRock and Dr. Brad Cookson of the University of Washington and published in the journal Cell Host & Microbe, believe their discoveries could potentially lead to the development of new vaccines for a range of infections.

"Many medical problems stem from too much or too little inflammatory reaction," Cookson said. "People who launch an insufficient inflammatory response, or whose inflammatory response is suppressed by medications, are prone to viral, bacterial and fungal infections.

The researchers found that Y. pestis secretes a leucine-rich protein that binds to and then disables the caspase-1 enzyme, which is then unable to signal the disease-fighting cells to self-destruct. Faulty capase-1 functioning has been implicated in a number of inflammatory disorders and understanding how pathogens manage its activity may provide clues to the development of new treatments, reports.

Currently, there is no vaccine against the plague, which is considered a potential biowarfare agent because it is extremely lethal when aerosolized. Respiratory forms of the illness damage the lungs and can spread further through coughs and sneezes.