Aberrant expression of selectin E, CXCL1, and CXCL13 in chronic endometritis

Abstract

Chronic endometritis is often identified in the patients with unexplained infertility, and is histopathologically characterized by infiltration of plasmacytes within the endometrial stroma. In parallel with stromal plasmacyte infiltration, the endometrial functional layer in chronic endometritis is invaded by B cells, which are a rare leukocyte subset residing within the basal layer in the nonpathological endometrium. In this study, we investigated the molecular expression underlying this unusual increase of B cells in chronic endometritis. Twenty-two out of 76 infertile patients were diagnosed with chronic endometritis from the stromal plasmacyte infiltration, and the endometrium contained numerous stromal B-cell aggregates and glandular single B cells. However, the other major leukocyte subsets, including T cells, natural killer cells, macrophages, and neutrophils were comparable in densities in chronic endometritis and nonpathological endometrium. The microvascular endothelium showed immunoreactivity to adhesion molecule selectin E and chemokine CXCL13 along with immunoreactivity to CXCL1 in the glandular epithelium in chronic endometritis, but not in the nonpathological endometrium. Lipopolysaccharide significantly induced surface selectin E expression and CXCL13 secretion in uterine microvascular endothelial cells, and CXCL1 secretion in endometrial epithelial cells in vitro. These findings indicated that the aberrant local microenvironment triggered possibly by bacterial infection has a role in selective extravasation of circulating B cells in chronic endometritis.