PuSH - Publication Server of Helmholtz Zentrum München

Aguilar-Pimentel, J.A. ; Cho, Y.-L. ; Gerlini, R. ; Calzada-Wack, J. ; Wimmer, M. ; Mayer-Kuckuk, P. ; Adler, T. ; Schmidt-Weber, C.B. ; Busch, D.H.* ; Fuchs, H. ; Gailus-Durner, V. ; Ollert, M.* ; Hrabě de Angelis, M. ; Ohlsson, C.* ; Poutanen, M.* ; Teperino, R. ; Strauss, L.*

Increased estrogen to androgen ratio enhances immunoglobulin levels and impairs B cell function in male mice.

Sci. Rep. 10:18334 (2020)
Publ. Version/Full Text Research data DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Sex steroids, such as estrogens and androgens, are important regulators of the humoral immune response. Studies in female mice have demonstrated that alteration of circulating estrogen concentration regulates antibody-mediated immunity. As males have normally little endogenous estrogen, we hypothesized that in males high estrogens and low androgens affect the immune system and enhance the allergic inflammatory response. Here, we studied transgenic male mice expressing human aromatase (AROM+). These animals have a high circulating estrogen to androgen ratio (E/A), causing female traits such as gynecomastia. We found that AROM+ male mice had significantly higher plasma immunoglobulin levels, particularly IgE. Flow cytometry analyses of splenocytes revealed changes in mature/immature B cell ratio together with a transcriptional upregulation of the Igh locus. Furthermore, higher proliferation rate and increased IgE synthesis after IgE class-switching was found. Subsequently, we utilized an ovalbumin airway challenge model to test the allergic response in AROM+ male mice. In line with above observations, an increase in IgE levels was measured, albeit no impact on immune cell infiltration into the lungs was detected. Together, our findings suggest that high circulating E/A in males significantly alters B cell function without any significant enhancement in allergic inflammation.
Altmetric
Additional Metrics?
Edit extra informations Login
Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
ISSN (print) / ISBN 2045-2322
e-ISSN 2045-2322
Quellenangaben Volume: 10, Issue: 1, Pages: , Article Number: 18334 Supplement: ,
Publisher Nature Publishing Group
Publishing Place London
Non-patent literature Publications
Reviewing status Peer reviewed
Grants Projekt DEAL