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Hematopoietic Remodeling in Interferon- -Deficient Mice
Infected With Mycobacteria
Peter J. Murray,
Richard A. Young, and
George Q. Daley
From the Whitehead Institute for Biomedical Research, Cambridge; and
the Department of Biology, Massachusetts Institute of Technology,
Cambridge, MA.
Control of intracellular bacterial infections requires
interferon- (IFN-) both for establishing a Th1 T-cell response
and for activating macrophages to kill the bacteria. Exposure of mice deficient in IFN- to mycobacterial infection produces an immune response characterized by a Th2 T-cell phenotype, florid bacterial growth, and death. We report here that IFN--deficient mice infected with mycobacteria also undergo a dramatic remodeling of the
hematopoietic system. Myeloid cell proliferation proceeds unchecked
throughout the course of mycobacterial infection, resulting in a
transition to extramedullary hematopoiesis. The splenic architecture of
infected IFN--deficient mice is completely effaced by expansion of
macrophages, granulocytes, and extramedullary hematopoietic tissue.
These features coincide with splenomegaly, an increase in splenic
myeloid colony-forming activity, and marked granulocytosis in the
peripheral blood. Systemic levels of cytokines are elevated,
particularly interleukin-6 (IL-6) and granulocyte colony-stimulating
factor (G-CSF). These results suggest that in addition to its central
role in cellular immunity, IFN- may be a key cytokine in coordinate
regulation of immune effector cells and myelopoiesis. This model should
be valuable for deciphering the cross-talk between the immune response
and hematopoiesis during bacterial infection and for improving our understanding of the mechanisms that control chronic infections.
Blood, Vol. 91 No. 8 (April 15), 1998:
pp. 2914-2924
© 1998 by The American Society of Hematology.
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