Journal of Leukocyte Biology
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Published online before print July 7, 2006
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0405201

Received for publication April 15, 2005.
Revised February 2, 2006.
Accepted for publication February 3, 2006.

Article

Interleukin-10 induces apoptosis in developing mast cells and macrophages

Daniel P. Bailey *, M. S. Mohit Kashyap *, L. Andrew Bouton *, Peter J. Murray {dagger}, and John J. Ryan *@

*Department of Biology, Virginia Commonwealth University, Richmond; and {dagger}Department of Infectious Diseases, St. Jude Children’s Research Hospital, Memphis, Tennessee

@ To whom correspondence should be addressed. E-mail: jjryan{at}saturn.vcu.edu.


  Abstract

Interleukin (IL)-10 is a potent immunoregulatory cytokine capable of inhibiting the inflammatory response. As mast cells are central effectors of inflammation, we investigated the effects of IL-10 on mast cell and macrophage development from mouse bone marrow progenitors. Bone marrow cells were cultured in IL-3 + stem cell factor (SCF), giving rise to mixed populations of mast cells and macrophages. The addition of IL-10 greatly decreased the expansion of bone marrow progenitor cells through a mechanism requiring signal tranducer and activator of transcription-3 expression. The inhibitory effects were a result of the induction of apoptosis, which occurred with caspase-3 activation and reduced mitochondrial membrane potential. Supporting a role for the mitochondrion, bone marrow cells from p53-deficient or Bcl-2 transgenic mice were partly resistant to the effects of IL-10. Further, IL-10 decreased Kit receptor expression and inhibited survival signaling by SCF or IL-3. These data indicate that IL-10 induces an intrinsic, mitochondrial apoptosis cascade in developing mast cells and macrophages through mechanisms involving blockade of growth factor receptor function. The ability of IL-10 to inhibit survival could support immune homeostasis by dampening inflammatory responses and preventing chronic inflammation.

Key Words: stat3 • hematopoietic • inflammation • caspase-3 • mitochondrial membrane potential • immune homeostasis




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