A role for leptin in sustaining lymphopoiesis and myelopoiesis
- Departments of *Food Science and Human Nutrition and
- †Biochemistry and Molecular Biology, Michigan State University, East Lansing, MI 48824-1319
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Contributed by Pamela J. Fraker, December 20, 2007 (received for review December 6, 2007)
Abstract
Although leptin is known for its regulation of food intake, it has many emerging roles in immune function. To better define the role of leptin in hematopoietic processes, a leptin-deficient obese mouse (ob/ob) and C57BL/6 lean wild-type controls were compared. Despite their large size and consumption of substantial amounts of nutrients, the ob/ob mice had only 60% as many nucleated cells in their marrow as controls. The greatest impact of leptin deficiency was on the B cell compartment that had 70% fewer cells, reducing the absolute number of pre-B and immature B cells to 21% and 12% of normal, respectively, and indicating a significant reduction in lymphopoiesis in ob/ob mice. Whereas the proportion of myeloids remained nearly normal in the obese mice, they also exhibited a reduction of 40% and 25%, respectively, in absolute numbers of granulocytes and monocytes. Seven days of provision of recombinant leptin promoted substantial lymphopoiesis, increasing the numbers of B cells in the marrow of the obese mice twofold, while doubling and tripling, respectively, the numbers of pre-B and immature B cells. Twelve days of supplementation brought these subpopulations to near-normal proportions. Leptin treatment also facilitated myelopoiesis such that the marrow of the obese mice contained normal numbers of monocytes and granulocytes after 7 days. Taken together, the data support an important role for leptin in sustaining lymphopoiesis and myelopoiesis.
Footnotes
- ‡To whom correspondence should be addressed. E-mail: fraker{at}msu.edu
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Author contributions: K.J.C., L.E.K., and P.J.F. designed research; K.J.C. and L.E.K. performed research; K.J.C., L.E.K., and P.J.F. analyzed data; and K.J.C. and P.J.F. wrote the paper.
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The authors declare no conflict of interest.
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This article contains supporting information online at www.pnas.org/cgi/content/full/0712053105/DC1.
- © 2008 by The National Academy of Sciences of the USA
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