"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."
Studies in mice with a chronic or long-term infection called Mycobacterium avium show that a greater proportion of a particular subset of their cells called long-term hematopoietic (blood-forming) stem cells are active. Gamma interferon prompts this activity. Mice that lack gamma interferon have fewer of these stem cells active during infection.
These findings show that gamma interferon not only activates stem cells during infection, but also regulate stem cells in normal times, enabling them to maintain the types of blood cells that exist in proportion or homeostasis.
"Our model predicts that bacterial infection detected by sentinel immune cells stimulates the increased release of gamma interferon, which then travels through the blood stream to activate HSCs (hematopoietic stem cells) in the bone marrow, leading to expansion and mobilization of the immune progenitor pool (the cells that ultimately produce immune system cells)," the researchers wrote.
They found that sustained activity by the hematopoietic stem cells can lead to at least transient problems with the quality of the stem cells and their abilities to stimulate production of more immune system cells.
"One of the most important things we found is th
|Contact: Glenna Picton|
Baylor College of Medicine