Dec 20, 2010 16:06 GMT  ·  By

A new investigation conducted by researchers in the United States has demonstrated the existence of a back-up plan of sorts for the human immune system, that kicks into gear when the usual processes underlying the body's natural defenses fail.

The newly-found system apparently kicks into gear to protect our organisms from infection and pathogens when the “master regulator” of the immune system can no longer function.

In a paper published in the December 19 online issue of the esteemed scientific journal Nature Immunology, experts at the University of California in San Diego (UCSD) School of Medicine give details about the “plan.”

They conducted the investigation together with colleagues from the Skaggs School of Pharmacy and Pharmaceutical Science, also at the university.

In past studies, it has been revealed that the nuclear factor kappa B (NF-κB) is one of the most important molecules in the body, underlying the actions of the innate immune system.

So researchers at UCSD decided to create mice in which to inhibit the expression of NF-κB. They then exposed the animals to pathogen-ridden conditions.

If the prevailing logic were to come out victorious, then the unsuspecting rodents should have been infected by a variety of pathogens. But UCSD distinguished professor of pharmacology Michael Karin says that that didn't happen.

In fact, the NF-κB-deficient mice proved more capable of clearing bacteria that cause a skin infection even more quickly than normal mice. This discovery hints at a hidden defense mechanism that may double the functionality of the immune system.

“We discovered that loss of NF-κB caused mice to produce a potent immune-activating molecule known as interleukin-1 beta (IL-1β), which in turn stimulated their bone marrow to produce dramatically increased numbers of white blood cells known as neutrophils,” Karin explains.

“Having a backup system in place is critical given the diverse strategies that bacterial pathogens have evolved to avoid bacterial clearance,” adds scientist Victor Nizet, MD.

“A number of bacteria are known to suppress pathways required for NF-κB activation, so IL-1β signaling could help us recognize and respond to these threats,” he adds.

Nizet holds an appointment as a professor of pediatrics and pharmacy at the university. His lab conducted the infectious challenge experiments in the new study.