M1 macrophages involved in the pathogenesis of placental chronic villitis of unknown etiology

2021 ◽  
pp. 1-6
Author(s):  
João Figueira Scarini ◽  
Natália de Magalhães Rodrigues ◽  
Wellington Lima Sabino ◽  
Ciro Soares ◽  
Thayná Melo de Lima Morais ◽  
...  
Keyword(s):  
Unknown Etiology ◽  
M1 Macrophages ◽  
Chronic Villitis

Immunohistochemical Study of M1 and M2 Macrophages Population in Chronic Villitis of the Placenta

2019 ◽  
Vol 152 (Supplement_1) ◽  
pp. S102-S102
Author(s):  
Erika Egal ◽  
Natalia de Magalhães Rodrigues ◽  
Fernanda Mariano ◽  
Reydson Souza ◽  
Joao Scarini ◽  
...  
Keyword(s):  
Tissue Repair ◽  
Etiologic Agent ◽  
Unknown Etiology ◽  
M2 Macrophages ◽  
M1 Macrophages ◽  
Effector Cells ◽  
Intervillous Space ◽  
M1 Phenotype ◽  
Chronic Villitis ◽  
M1 And M2 Macrophages

Abstract Introduction Villitis is characterized by the presence of inflammatory infiltrate (CD8 lymphocyte) in the placental villous and is classified as to the etiology in known and unknown. In most cases, villitis is idiopathic (villitis of unknown etiology [VUE]) because no microorganisms are evident and there are no maternal symptoms or signs. It has recently been proposed that pregnancy is, in fact, an active and highly regulated immune process in which macrophages play an important role. Macrophages may present with M1 phenotype, important effector cells, or M2 phenotype, capable of suppressing the function of M1 macrophages and influencing immunoregulation and tissue repair. CD68 antibody recognizes macrophages M1 and M2, whereas CD11c and CD163 antibodies are specific for the identification only of M1 and M2 macrophages, respectively. The objective of our study is to characterize in human placentas in the subpopulation of M1 and M2 macrophages in VUE. Methods Sixteen cases of chronic villitis (all without an identifiable etiologic agent) and three control placentas were examined using immunohistochemistry with antibodies for CD68, CD11c, CD163, and CD3. Results CD68 and CD163 were present in all cases in the normal areas. CD68, CD163, and CD11c were present in the villous stroma and in the intervillous space in the inflamed areas. The percentage of CD68-positive macrophages was higher than CD163- and CD11c-positive macrophages in all specimens studied. A total increase of CD68, CD163, and CD11c with the predominance of CD11c over CD163 in the inflamed areas was observed. Conclusion The predominance of M1 macrophages (CD11c) in the inflamed areas suggests the influence of these cells in the pathogenesis VUE. The higher amount of M2 (CD163) in the inflamed villous compared to normal areas suggests a possible immunoregulatory mechanism of the inflammatory process in VUE.

Perinatal prognosis of pregnancies complicated by placental chronic villitis or intervillositis of unknown etiology and combined lesions: About a series of 178 cases

Placenta ◽  
2016 ◽  
Vol 44 ◽  
pp. 104-108 ◽  
Author(s):  
Christel Nowak ◽  
Madeleine Joubert ◽  
Frederique Jossic ◽  
Agathe Masseau ◽  
Mohamed Hamidou ◽  
...  
Keyword(s):  
Unknown Etiology ◽  
Combined Lesions ◽  
Chronic Villitis

Seasonal Variation of Chronic Villitis of Unknown Etiology

2019 ◽  
Vol 23 (4) ◽  
pp. 253-259
Author(s):  
Alexa A Freedman ◽  
Jeffery A Goldstein ◽  
Gregory E Miller ◽  
Ann Borders ◽  
Lauren Keenan-Devlin ◽  
...  
Keyword(s):  
Seasonal Variation ◽  
Inflammatory Lesion ◽  
Unknown Etiology ◽  
Low Grade ◽  
Text Search ◽  
Standardized Protocol ◽  
Prevalence Estimates ◽  
Chronic Villitis ◽  
Pathology Reports ◽  
Estimate Prevalence

Introduction Chronic villitis of unknown etiology (VUE) is a chronic inflammatory lesion of the placenta. VUE is hypothesized to result from an alloimmune response or as response to an unidentified infection. Lack of a seasonal trend is thought to support VUE as an alloimmune response, though data on seasonal VUE trends are limited. Methods Data were obtained from a hospital in Chicago, Illinois, from 2011–2016. Placentas sent to pathology were reviewed using a standardized protocol, and VUE cases were identified based on an automated text search of pathology records. We used monthly VUE prevalence estimates to investigate the annual trend, and we used Poisson regression to evaluate seasonal variation in the number of VUE cases. Results There were 79 825 deliveries within the study period. Pathologists evaluated 12 074 placentas and identified 2873 cases of VUE. Regression results indicate that the risk of VUE is 16% to 17% higher in the fall and winter as compared to the summer (fall relative risk [RR]: 1.17, 95% confidence interval [CI]: 1.06–1.29; winter RR: 1.16, 95% CI: 1.05–1.29). Discussion Our results suggest that there may be seasonal variation in VUE prevalence, particularly for low-grade VUE. Future studies should evaluate seasonal variation in a representative sample rather than relying on pathology reports to estimate prevalence.

Histological Features of Shallow Placental Implantation Unify Early-Onset and Late-Onset Preeclampsia

2018 ◽  
Vol 22 (2) ◽  
pp. 112-122 ◽  
Author(s):  
Jerzy Stanek
Keyword(s):  
Early Onset ◽  
Late Onset ◽  
Unknown Etiology ◽  
Hypertension In Pregnancy ◽  
Pathological Mechanism ◽  
Comparative Group ◽  
Laminar Necrosis ◽  
Chronic Villitis ◽  
Early Onset Preeclampsia ◽  
In Pregnancy

Preeclampsia is distinguishable from other hypertensive conditions of pregnancy by its high rates of decidual arteriopathy, the uterine type of chronic hypoxic placental injury, the occurrence of villous infarctions, and clusters of multinucleate trophoblasts in the maternal floor. To retrospectively study the clinical and placental phenotypes of 230 women with early-onset preeclampsia, 261 women with late-onset preeclampsia, and 5059 women without hypertension in pregnancy (comparative group), 24 clinical and 46 placental phenotypes were statistically compared (analysis of variance, χ2 with Bonferroni correction). The frequency of decidual arteriopathy (both hypertrophic and atherosis), patterns of chronic hypoxic placental injury, villous infarction, membrane laminar necrosis, membrane microscopic chorionic pseudocysts, clusters of maternal floor multinucleated trophoblasts, excessive number of extravillous trophoblasts, and intervillous thrombi was strikingly higher in both late-onset preeclampsia and early-onset preeclampsia than in the comparative group without hypertension in pregnancy. All 3 patterns of chronic hypoxic placental injury were 2- to 3-fold more common in preeclampsia. Although the preuterine pattern was as common in early-onset preeclampsia as it was in late-onset preeclampsia, the postuterine pattern was 2-fold more common in early-onset preeclampsia, and chronic villitis of unknown etiology was more common in late-onset preeclampsia than in the other 2 groups. Features of shallow placental implantation occurred at the same frequency in early-onset preeclampsia as in late-onset preeclampsia, which reflects an underlying common pathological mechanism in both subgroups of preeclampsia, while hypoxic lesions and patterns of placental injury were more common in early-onset preeclampsia than in late-onset preeclampsia, which correlates with more severe clinical outcomes of the former.

Characterization of Inflammation in Syphilitic Villitis and in Villitis of Unknown Etiology

2004 ◽  
Vol 7 (5) ◽  
pp. 453-458 ◽  
Author(s):  
Payal Kapur ◽  
Dinesh Rakheja ◽  
Ana M. Gomez ◽  
Jeanne Sheffield ◽  
Pablo Sanchez ◽  
...  
Keyword(s):  
Relative Number ◽  
Lymphocytic Infiltrate ◽  
Unknown Etiology ◽  
Histologic Diagnosis ◽  
Cd8 Cells ◽  
Y Chromosomes ◽  
Hla Dr ◽  
Chronic Villitis ◽  
Undetermined Etiology ◽  
Infiltrating Lymphocytes

Chronic villitis is a histologic diagnosis that may be either associated with infection, or termed villitis of undetermined etiology (VUE). The lymphocytic infiltrate in VUE has been reported to consist of maternal lymphocytes, but the origin of the lymphocytic infiltrate in infectious villitis has not been identified. The purpose of our study was to compare the maternal vs. fetal origin of the infiltrating lymphocytes in VUE and syphilitic villitis, and to expand the immunophenotypic data provided by previous studies. Paraffin-embedded placentas from four males with VUE and two males with syphilitic vil litis were subjected to fluorescence in situ hybridization (FISH) for the X and Y chromosomes. Serial sections were stained with antibodies to CD3, CD4, CD8, CD68, HLA-DR, and CD20. Quantitation of the relative number of cells marking with each antibody was done for four villi in each slide. CD3 lymphocytes predominated in both VUE and syphilitic villitis, with slightly more CD8 cells compared to CD4 cells. CD68 and HLA-DR positive cells were as frequent as CD3 cells, and B-lymphocytes were rare. Maternal cells were the predominant intravillous population in both VUE and syphilitic villitis, and neutrophils in syphilitic villitis were also maternal. These data indicate that the immune response in both syphilitic villitis and VUE is similar, raising the possibility of a similar immunopathogenetic pathway.

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