Osteoporosis induced in mice by overproduction of interleukin 4.

Abstract

Osteoporosis is a common disease in which loss of bone mass results in skeletal fragility. The development of therapies for this disorder has been hampered by the lack of a convenient animal model. Here we describe a disorder in bone homeostasis in transgenic mice that inappropriately express the cytokine interleukin 4 (IL-4) under the direction of the lymphocyte-specific proximal promoter for the lck gene. Bone disease in lck-IL-4 mice appeared to result from markedly decreased bone formation by osteoblasts, features strikingly similar to those observed in cases of severe low-turnover human involutional osteoporosis. By 2 months of age, female and male lck-IL-4 mice invariably developed severe osteoporosis of both cortical and trabecular bone. Osteoporosis was observed in two independently derived founder animals, indicating that this phenotype was directly mediated by the IL-4 transgene.

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@article{Lewis1993OsteoporosisII, title={Osteoporosis induced in mice by overproduction of interleukin 4.}, author={David B Lewis and H. Denny Liggitt and Eric L. Effmann and S. Timothy Motley and Steven L Teitelbaum and Karl J . Jepsen and Steve A.N. Goldstein and Jeffrey F. Bonadio and James E. Carpenter and Roger M. Perlmutter}, journal={Proceedings of the National Academy of Sciences of the United States of America}, year={1993}, volume={90 24}, pages={11618-22} }