Most of the time, the body's blood-forming (hematopoietic) stem cells remain dormant, with just a few producing blood cells and maintaining a balance among the different types.
However, invading bacteria can be a call-to-arms, awaking the sleeping stem cells and prompting them to produce immune system cells that fight the foreign organisms. The "bugler" that awakes the stem cells in this battle is gamma interferon, a front-line protein defender against bacterial infection, said researchers from Baylor College of Medicine (www.bcm.edu) in a report that appears in the current issue of the journal Nature (www.nature.com).
"We are looking at the normal function of stem cells," said Dr. Margaret Goodell (www.bcm.edu/star/index.cfm?pmid=2947), professor of molecular and human genetics at BCM and director of the Stem Cells and Regenerative Medicine (STaR) (www.bcm.edu/star/index.cfm?PMID=0) Center. She is the report's senior author. "One of those is to respond to an infection."
Goodell and her colleagues knew that cells farther along in the differentiation process responded to infection, increasing the production of immune cells.
"We were sure there was a mechanism by which hematopoietic stem cells respond to infection, but it was not obvious," she said. They started their work with gamma interferon because they knew it played an important role in bacterial infection.
The collaboration and talents of two researchers in her laboratory - first co-authors Drs. Megan T. Baldridge and Katherine Y. King - facilitated the work with mice that led to this finding, said Goodell. Both are at BCM.
"I think our findings represent an exciting new avenue for studying hematopoiesis," said King. "By viewing the hematopoietic stem cell as the source of the immune system, we are finding fundamental ways in which the immune response affects bone marrow. This is the first time that anyone has extensively studied hematopoietic stem cells in the context of an in vivo model (a living organism) of infection."
"As a specialist in infectious diseases, I see many patients whose bone marrow no longer produces sufficient blood cells as a consequence of their infection. This is particularly relevant in chronic infections such as mycobacterial diseases (that include tuberculosis) and AIDS," said King. "Our studies lend insight into the causes of this decrease in bone marrow function during such infections, and I hope the work will someday lead to new therapies."