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Updated: Aug 12, 2026
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A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders
Published on: June 8, 2014
Increased in vitro bone resorption by monocytes in the hyper-immunoglobulin E syndrome
D Y Leung1, L Key, J J Steinberg
1Division of Allergy, Children's Hospital, Boston, MA 02115.
Journal of Immunology (Baltimore, Md. : 1950)
|January 1, 1988
Summary
Children with hyper-immunoglobulinemia E syndrome exhibit low bone density and increased bone resorption. Monocytes from these patients show heightened activity, potentially driven by prostaglandin pathways, contributing to bone loss.
Area of Science:
- Immunology
- Bone Biology
- Genetics
Background:
- Hyper-immunoglobulinemia E syndrome (HIES) is a primary immunodeficiency associated with recurrent infections and eczema.
- Patients with HIES are known to be prone to bone fractures, suggesting underlying bone density issues.
Purpose of the Study:
- To investigate the bone density and monocyte function in patients with HIES.
- To explore the mechanisms contributing to osteopenia in HIES.
Main Methods:
- Bone density was measured using photon absorptiometry in six HIES patients.
- In vitro bone degradation assays were performed using peripheral blood monocytes.
- Prostaglandin E2 levels and the effect of indomethacin and aspirin on bone resorption were assessed.
Main Results:
- All six HIES patients had significantly reduced bone density compared to controls.
- Monocytes from HIES patients showed significantly higher bone degradation capacity.
- Elevated prostaglandin E2 release by monocytes was observed, and indomethacin/aspirin reduced bone resorption.
Conclusions:
- Monocytes in HIES patients are activated for bone resorption via the prostaglandin synthase pathway.
- This monocyte-mediated bone resorption may contribute to the osteopenia observed in HIES.
- Targeting prostaglandin synthesis could be a therapeutic strategy for bone complications in HIES.
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