Hormonal Regulation of Immunoglobulins in the Rat Uterus: Uterine Response to a Single Estradiol Treatment*

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Abstract
Levels of immunoglobulin (Ig) A and IgG were analyzed in uterine tissue and secretions to examine the mechanisms by which estrogens regulate luminal Ig accumulation. Within 3 h after a single injection of estradiol (1 μg) to ovariectomized rats, levels of both IgA and IgG increased significantly in uterine tissue. Ig content remained elevated at 6 h and then declined by 22 h after estradiol treatment. These rapid increases in tissue levels of IgA and IgG were dose dependent and were accompanied by elevations in tissue IgM and total protein content. Analysis of uterine secretions demonstrated that estradiol also significantly increased the levels of luminal IgG, relative to control, but had no effect on either IgA or IgM. Luminal IgG content rose significantly within 3 h after a single estradiol treatment and decreased to control levels by 22 h. The amounts of IgG in uterine secretions at 3 and 6 h were significantly less than IgG levels measured in uterine tissue. The pattern of protein accumulation in the uterine lumen after estradiol administration was analogous to that of IgG. Since Ig accumulation occurred in parallel with uterine water imbibition, our findings suggest that the rapid increases in tissue IgA, IgG, and IgM after estradiol treatment are due to serum transudation and not local synthesis. This conclusion is supported by several observations. First, immunofluorescent studies failed to demonstrate the presence of IgA-positive cells in uterine tissue 3 h after estradiol administration. Second, radiolabeled IgG moved from blood to uterine tissue to lumen during water imbibition. The [125I]IgG specific activities in both serum and tissue were identical. Third, estriol treatment of ovariectomized rats duplicated the rapid effects of estradiol on uterine weight and tissue and luminal IgG accumulation. Fourth, when dexamethasone was administered before estradiol, both the wet weight elevation and the uterine IgG response were blocked. These experiments indicate that estrogens exert a rapid effect on uterine Ig levels through a process that involves serum transudation. Furthermore, these findings show that the mechanisms responsible for IgG and IgA movement into the uterine lumen after estrogen treatment are different.