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Orally administered interferons suppress bone marrow function

S Koren1, W R Fleischmann

  • 1Department of Microbiology, University of Texas Medical Branch, Galveston 77555.

Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)
|November 1, 1993
PubMed
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Oral interferon administration suppresses bone marrow function similarly to subcutaneous routes, offering potential for treating myelogenous diseases. This bone marrow suppression is distinct from antibody-mediated mechanisms seen with subcutaneous interferons.

Area of Science:

  • Immunology
  • Pharmacology
  • Hematology

Background:

  • Interferons (IFNs) are clinically administered via multiple routes, including intramuscular, subcutaneous, and intravenous.
  • Recent studies indicate oral interferon administration suppresses peripheral white blood cell (WBC) counts through a distinct mechanism compared to intraperitoneal routes.

Purpose of the Study:

  • To investigate if oral interferon treatment induces bone marrow suppression.
  • To characterize and compare the bone marrow-suppressive effects of oral and subcutaneous recombinant human IFN-alpha A/D (rHuIFN-alpha A/D) with their peripheral WBC-suppressive effects.

Main Methods:

  • Kinetics studies were performed to characterize the bone marrow-suppressive effects of orally and subcutaneously administered rHuIFN-alpha A/D.
  • Peripheral WBC counts and bone marrow function were monitored following administration of rHuIFN-alpha A/D via oral and subcutaneous routes.

Related Experiment Videos

  • Mechanisms of bone marrow suppression were investigated by comparing the effects of subcutaneous and oral murine IFN-alpha/beta (MuIFN-alpha/beta) in the presence of anti-IFN antibodies.

    • Main Results:

    • Both oral and subcutaneous rHuIFN-alpha A/D significantly suppressed peripheral WBC counts and bone marrow function within 1 day, reaching maximum suppression by 3 days and plateauing over 12 days.
    • The WBC-suppressive and bone marrow-suppressive effects of oral and subcutaneous rHuIFN-alpha A/D paralleled each other and diminished at the same rate after treatment cessation, with suppression lost by 5 days.
    • Bone marrow suppression by subcutaneous MuIFN-alpha/beta was blocked by antibodies, whereas oral MuIFN-alpha/beta-induced bone marrow suppression occurred even in the presence of antibodies.

    Conclusions:

    • Oral interferon administration induces bone marrow suppression comparable to subcutaneous administration.
    • The mechanisms underlying bone marrow suppression differ between oral and subcutaneous interferon administration, with oral routes not being blocked by antibodies.
    • These findings support the potential clinical utility of oral interferons, particularly for managing myelogenous diseases.