A molecule known as nuclear factor kappa B (NF-?B) has been regarded as the "master regulator" of the body's innate immune response, receiving signals of injury or infection and activating genes for microbial killing and inflammation.
Scientists at the University of California, San Diego School of Medicine and Skaggs School of Pharmacy and Pharmaceutical Sciences studied the immune function of laboratory mice in which genetic tools were used to block the pathway for NF-?B activation.
The researchers made the unexpected and counterintuitive discovery that NF-?B-deficient mice were able to clear bacteria that cause a skin infection even more quickly than normal mice.
"We discovered that loss of NF-?B caused mice to produce a potent immune-activating molecule known as interleukin-1 beta (IL-1_), which in turn stimulated their bone marrow to produce dramatically increased numbers of white blood cells known as neutrophils," said lead author Michael Karin, Distinguished Professor of Pharmacology.
The new research demonstrates that the innate immune system deploys two effective strategies to deal with invasive bacterial infection, and that the IL-1_ system provides an important safety net when NF-?B falls short.
The study appeared in the December 19 online issue of the journal Nature Immunology.