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Visualization of Estrogen Receptors in Colons of Mice with TNBS-Induced Crohn's Disease using Immunofluorescence

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Estrogen metabolism and autoimmunity.

Maurizio Cutolo¹, Alberto Sulli, Rainer H Straub

¹Research Laboratory and Academic Unit of Clinical Rheumatology, Dept. Internal Medicine, University of Genova Italy, Viale Benedetto XV, 6-16132 Genova, Italy. mcutolo@unige.it

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Summary

Estrogen metabolites, not serum levels, drive autoimmune rheumatic diseases by promoting cell proliferation and cytokine production in immune cells. Elevated 16alpha-hydroxylated estrogens are linked to synovial inflammation.

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Area of Science:

Immunology
Endocrinology
Rheumatology

Background:

Estrogens influence humoral immunity and autoimmune rheumatic diseases.
Peripheral estrogen metabolites, rather than serum levels, are key in disease pathophysiology.
Accelerated aromatase-mediated conversion of androgens to estrogens occurs in inflamed tissues.

Purpose of the Study:

Investigate the role of peripheral estrogen metabolites in autoimmune rheumatic diseases.
Clarify the intracrine effects of estrogen metabolites on immune cells.
Determine the significance of specific estrogen metabolites in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE).

Main Methods:

Analysis of estrogen metabolism in peripheral tissues.
Assessment of estrogen metabolite effects on immune cell proliferation and cytokine production.
Comparison of urinary estrogen levels in healthy subjects versus patients with RA and SLE.

Main Results:

Intracrine synthesis of estrogen metabolites in macrophages and fibroblasts stimulates cell proliferation and tumor necrosis factor (TNF) production in RA synovial tissue.
16alpha-hydroxylated estrogens, such as 16alpha-hydroxyestrone, promote cell proliferation and interfere with monocyte proliferation.
Healthy subjects exhibit significantly higher urinary concentrations of 2-hydroxyestrogens compared to RA or SLE patients.

Conclusions:

Intracrine estrogen metabolite synthesis is a common pathway in immune cells, influencing immune reactivity in both sexes.
A preponderance of 16alpha-hydroxylated estrogens is associated with synovial inflammation and hyperplasia.
Altered estrogen metabolism, particularly reduced 2-hydroxyestrogen excretion, may be a biomarker for autoimmune rheumatic diseases.