Association between chronic endometritis and uterine natural killer cell density in women with recurrent miscarriage: clinical implications

Abstract

Aim: This aim of this study was to determine the association between uterine natural killer (uNK) cell density and chronic endometritis (CE). Methods: Endometrial biopsies from 135 women with recurrent miscarriage were obtained precisely 7 days after luteinizing hormone surge in natural cycles. Endometrial sections were immunostained for CD56 for uNK cells and CD138 for plasma cells, respectively. Uterine NK cell counting was performed according to a standardized protocol and results were expressed as percentage of CD56+ cells/ total stromal cells. High uNK cell density was defined as >4.5% and CE was diagnosed when the plasma cell density > 5.15 cells/ 10 mm 2 . Results: The uNK cells density in women with CE (median, 5.1%; range, 3.4-8.8%) was significantly (P < 0.05) higher than that of those without CE (median, 3.8%; range, 1.2%-7.3%). The prevalence of high uNK cell density in women with CE (11/29, 37.9%) was significantly (P < 0.05) higher than that of women without CE (8/106, 7.5%). Conclusion: To conclude, there was a significant association between high uNK cell density and CE. In women with high uNK cell density, plasma cell should be examined to determine if the underlying cause is associated with CE.

METTL3-Mediated m6A RNA Methylation of ZBTB4 Interferes With Trophoblast Invasion and Maybe Involved in RSA

“…Studies have shown that TLR was expressed in placental cells and participated in the initiation of signal mediators that were essential for the immune response in choriocarcinoma cell lines, which may be related to placental inflammation ( Klaffenbach et al, 2005 ). Similarly, cytotoxicity mediated by natural killer cells (NK) can lead to endometritis, form a uterine immune state, and then lead to infertility, recurrent abortion, and so on ( Chen et al, 2020 ; Li et al, 2020 ; Gu et al, 2021 ). Other studies have shown that apoptosis can affect the differentiation and invasion of trophoblast cells, block the process of vascular recasting, change the function of the placenta, and finally lead to embryo implantation, growth restriction, and abortion ( Sharp et al, 2010 ).…”

“…In this study, we found that m 6 A modification in RSA trophoblast cells was significantly different from that in the normal control group through MeRIP-seq, and the pathways of the differential m 6 A modified genes enriched have been reported to be related to the pathogenesis of RSA such as toll-like receptor signaling pathway, natural killer cell–mediated cytotoxicity, and necrotizing apoptosis. ( Klaffenbach et al, 2005 ; Sharp et al, 2010 ; Chen et al, 2020 ; Li et al, 2020 ; Gu et al, 2021 ). The authors pointed out that URSA patients, compared with normal pregnant women, were enriched in several signaling pathways associated with immune regulatory functions, including natural killer cell–mediated cytotoxicity, cytokine receptor interaction, and other signaling pathways which were consistent with our findings ( Klaffenbach et al, 2005 ; Sharp et al, 2010 ; Chen et al, 2020 ; Li et al, 2020 ; Gu et al, 2021 ).…”

“…( Klaffenbach et al, 2005 ; Sharp et al, 2010 ; Chen et al, 2020 ; Li et al, 2020 ; Gu et al, 2021 ). The authors pointed out that URSA patients, compared with normal pregnant women, were enriched in several signaling pathways associated with immune regulatory functions, including natural killer cell–mediated cytotoxicity, cytokine receptor interaction, and other signaling pathways which were consistent with our findings ( Klaffenbach et al, 2005 ; Sharp et al, 2010 ; Chen et al, 2020 ; Li et al, 2020 ; Gu et al, 2021 ).…”

Recurrent Implantation Failure: Bioinformatic Discovery of Biomarkers and Identification of Metabolic Subtypes

“…An inflammatory process within the endometrium may cause cellular and biochemical alterations, leading to the risk of RIF. Endometrial inflammation changes the mechanisms securing the timely arrival of a viable blastocyst in a receptive endometrium [33]. Studies have demonstrated that the expression of the genes potentially associated with embryo receptivity and decidualization is likely downregulated in the endometrium in RIF cases with chronic endometritis [34].…”

Endometrial causes of recurrent pregnancy losses: endometriosis, adenomyosis, and chronic endometritis

“…An inflammatory process within the endometrium may cause cellular and biochemical alterations. Endometrial inflammation alters the mechanisms securing the timely arrival of a viable blastocyst in a receptive endometrium during the WOI (142). In humans, the endometrium undergoes a series of changes leading to embryo receptivity during a limited period, normally occurring 5 to 7 days after ovulation and lasting for about 4 days (cycle days 20-24) during the WOI (143).…”