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Research Article Free access | 10.1172/JCI116528

Hormonal control of intestinal Fc receptor gene expression and immunoglobulin transport in suckling rats.

M G Martín, S V Wu, and J H Walsh

Center for Ulcer Research and Education, University of California, Los Angeles.

Find articles by Martín, M. in: PubMed | Google Scholar

Center for Ulcer Research and Education, University of California, Los Angeles.

Find articles by Wu, S. in: PubMed | Google Scholar

Center for Ulcer Research and Education, University of California, Los Angeles.

Find articles by Walsh, J. in: PubMed | Google Scholar

Published June 1, 1993 - More info

Published in Volume 91, Issue 6 on June 1, 1993
J Clin Invest. 1993;91(6):2844–2849. https://doi.org/10.1172/JCI116528.
© 1993 The American Society for Clinical Investigation
Published June 1, 1993 - Version history
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Abstract

Hormonal control of immunoglobulin (Ig) absorption and of intestinal Fc receptor mRNA expression were investigated in rats to assess its potential role in the normal postsuckling inhibition of this transport system. Corticosterone and L-thyroxine therapy caused premature inhibition of the absorption of orally administered murine monoclonal antibody and of Fc receptor mRNA expression in a dose- and time-dependent manner. Low-dose corticosterone had no effect on Fc receptor mRNA synthesis after 3 d but decreased Ig transport fivefold after 7 d. High dose corticosterone resulted in a threefold reduction in Fc receptor after 3 d, and there was almost complete inhibition (> 30-fold) of transport and of Fc receptor transcript levels after 7 d. Similarly, 7 d of high-dose thyroxine decreased both serum Ig transport and Fc receptor (> 30-fold). However, adrenalectomy did not prevent the normal post-suckling declines in Ig transport or receptor synthesis. This study demonstrates that exogenous corticosteroids and thyroxine hormone inhibit Ig transport and steady-state duodenal Fc receptor mRNA levels in suckling rats. Endogenous adrenal steroids however, do not appear to be entirely responsible for the age-dependent decline in this transport system.

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