It is an acknowledged fact that SARS-CoV-2 exhibits tropism for the human placenta. A possible mechanism of SARS-CoV-2 entry into host cells is via angiotensin-converting enzyme 2 (ACE2) receptors, which are expressed in trophoblasts, endothelial cells, and macrophages. The present study describes a case of spontaneous miscarriage in the 20th gestational week after maternal SARS-CoV-2 infection. The placenta and various fetal organs were examined for structural alterations and expression of the viral nucleocapsid protein and several immune cell markers via immunohistochemistry (IHC). Histopathological examination of the placenta revealed acute chorioamnionitis, acute subamnionic placentitis, multiple intervillous thrombi, increased fibrinoid deposition, and necrotic changes of the chorionic villi. Immunohistochemistry confirmed the presence of SARS-CoV-2 nucleocapsid protein regions predominantly in the syncytiotrophoblast. Staining of the placental tissue for different markers helped elucidate the distribution of immune cells. Pathomorphological examination of the fetal organs demonstrated changes in microcirculation with the presence of sludge phenomenon and diapedesis haemorrhages, mostly in the lungs, brain, and myocardium. IHC staining of fetal organs revealed expression of SARS-CoV-2 nucleocapsid protein, which was detected to the highest extent in the brain, lungs, and liver. The findings of the present report support the hypothesis of possible vertical transmission of SARS-CoV-2 from mother to fetus.

Adenomyosis and endometriosis are distinct gynecological disorders characterized by ectopic growth of endometrial tissue. Their etiology remains unclear, but stem cells have been implicated in both. The aim of this study was to investigate and compare the quantity of NOTCH1+ and CD117+ stem cells in endometriosis and adenomyosis lesions. Immunohistochemical staining of ectopic endometrium biopsies using antibodies against NOTCH1 and CD117 was performed. The quantity and spatial distribution of endometrial stromal cells positive for these markers were determined and compared between endometriosis and adenomyosis lesions. Additionally, their quantities were compared between endometriosis lesion types. Mann–Whitney U test showed that the median percentages of both NOTCH1+ and CD117+ cells in the endometriosis lesions were significantly higher than those in the adenomyosis lesions (2.26% vs. 0.13%, p = 0.002 and 0.44% vs. 0.26%, p = 0.016, respectively). Spearman’s test showed a positive correlation between NOTCH1+ and CD117+ cells in endometriosis lesions (R = 0.45, p = 0.027) but no significant correlation in adenomyosis lesions (R = −0.11, p = 0.69). The quantity of both stem cell types was highest in extragenital endometriotic lesions. Unlike adenomyosis, endometriosis lesions are associated with higher quantities of NOTCH1+ and CD117+ stem cells and a coordinated increase in their number. These findings support the distinct origin of the two conditions.

Background/Objectives: Senescent cells contribute to endometrial remodeling during the implantation window, but their spatial organization within the stroma remains poorly understood. This study aimed to characterize the distribution of senescent (p16-positive) cells in the functional layer of the endometrium and to evaluate their spatial relationships with immune cell subsets. Methods: Endometrial biopsies from 68 women undergoing IVF were collected during the mid-luteal phase (LH+7, corresponding to the implantation window). Samples were analyzed by immunohistochemistry for p16 and immune markers (CD3, CD4, CD8, CD14, CD68, CD56, CD79α). Images from adjacent serial sections were digitally aligned, and senescent cell density, clustering, and nearest-neighbor distances to immune cells were quantified using HALO Image Analysis software (v3.4). Ratios of senescent-to-immune cell abundance were also calculated to account for stromal variability. Results: Senescent cells were heterogeneously dispersed within the stroma, with occasional high-density clusters. Quantitative analysis revealed that their abundance was lower than that of monocytes, macrophages, and total T cells, but higher than that of T-helper and B cells. Across patients, median senescent-to-immune cell ratios were approximately 1, indicating comparable abundances, except for CD4⁺ and CD79α⁺ subsets, where ratios were significantly elevated. Nearest-neighbor analysis showed that macrophages and monocytes localized in closest proximity to senescent cells (45 ± 20 μm and 45 ± 25 μm), while T-helper and NK cells were positioned at greater distances from senescent cells (102 ± 42 μm and 53 ± 23 μm, respectively). B cells showed the greatest separation (211 ± 66 μm). Correlation analysis confirmed density-driven proximity for most immune subsets, with CD4⁺ and CD56⁺ cells as exceptions, displaying limited spatial association with senescent cells. Conclusions: Senescent cells in the endometrium during the implantation window display heterogeneous distribution and selective spatial associations with immune subsets. Their preferential distancing from T-helper and NK cells suggests impaired local immune–senescence crosstalk, highlighting spatial profiling of senescent cells as a potential diagnostic marker of endometrial receptivity.

Successful implantation requires a finely regulated endometrial microenvironment during the window of implantation. Chronic endometritis, defined by plasma cell infiltration, and stromal senescence, indicated by p16 expression, represent separate but potentially interacting mechanisms associated with impaired endometrial receptivity. The relationship between these processes remains poorly understood. We aim to examine whether stromal senescence is associated with plasma cell density and clustering in the human endometrium during the implantation window. Forty mid-luteal (LH+7) endometrial biopsies were retrospectively analyzed and stratified into low-senescence (3.5%, n = 20) groups. Plasma cells were identified by immunohistochemistry for MUM1 and CD138 and quantified using HALO^® software (version 3.4). Group comparisons were performed using Student’s t-test and chi-squared analysis. CD138⁺ plasma cells were significantly more abundant in high-senescence endometria than in low-senescence controls (0.065 ± 0.10 vs. 0.014 ± 0.027 cells/mm², p = 0.02). Only MUM1⁺ cells formed stromal clusters, which were more frequent in high-senescence samples (67% vs. 31%, p = 0.05). High endometrial stromal senescence during the implantation window is associated with increased plasma cell infiltration and clustering. This interplay may contribute to chronic endometritis and impaired receptivity, providing new insights into potential diagnostic and therapeutic strategies for reproductive failure.