Search PubMedSearch

SEARCH · Search PubMed

Results for “Chorioamnionitis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

8 recordsLinked to original sources

Intramembranous localization of bacteria in beta-hemolytic group B streptococcal chorioamnionitis.

An unusual pathologic finding consisting of large colonies of bacteria, localized immediately beneath the epithelial layer of the amnion, has been observed in association with an example of group B beta-hemolytic streptococcal chorioamnionitis. Postpartum endometritis as well as neonatal sepsis and meningitis occurred. Histologic examination of the umbilical cord and placenta revealed routine features of intraamniotic inflammation, but the membranes were characterized by the presence of unusual darkly staining deposits of material immediately beneath the amniotic epithelium. Subsequent special stains revealed these to be colonies of gram-positive cocci. We have been unable to find a previous description of this observation in association with streptococcal or with other types of chorioamnionitis.

Adult

MicroRNA-155 modulates STAT3 signaling by targeting KPNA1 in chronic chorioamnionitis of human placenta.

Chronic chorioamnionitis (CCA) is a placental inflammatory lesion characterized by maternal T cell infiltration and trophoblast apoptosis, resembling allograft rejection. MicroRNA-155 (miR-155) is a central regulator of immune and inflammatory pathways, but its role in CCA remains unclear. This study investigated whether miR-155 contributes to the pathogenesis of CCA by targeting karyopherin α1 (KPNA1) and modulating STAT3 signaling in human trophoblasts. Placental tissues from 28 CCA cases and 16 gestational age-matched controls were analyzed for miR-155 expression using quantitative RT-PCR and in situ hybridization. Functional assays were conducted in Swan 71 trophoblast cells following miR-155 overexpression and siRNA-mediated KPNA1 knockdown. Microarray and qRT-PCR analyses identified gene expression changes, while western blotting and dual-luciferase reporter assays were conducted to evaluate STAT3 activity and direct target binding. miR-155 expression was significantly elevated in CCA fetal membranes. KPNA1 was identified as a direct target of miR-155, and its suppression reduced STAT3 phosphorylation and nuclear translocation. Dual-luciferase assays confirmed that miR-155 binds to the 3' untranslated region of KPNA1 mRNA, thereby inhibiting its translation. These findings suggest that miR-155 downregulates KPNA1, leading to inhibition of STAT3 signaling in trophoblasts, which may contribute to maternal-fetal immune dysregulation and trophoblast apoptosis in CCA. The miR-155-KPNA1-STAT3 axis may represent a potential therapeutic target in pregnancy-related inflammatory disorders.

Humans

Pathology of the placenta and cord in ascending and in haematogenous infection.

The two main patterns of inflammatory response in the placenta and its adnexae are: (1) amniotic infection, usually bacterial ascending, with acute chorioamnionitis and funisitis; (2) haematogenous villitis, usually viral, with early necrotizing lesions and vasculitis and, later, chronic infiltrates and obliterative vasculitis. In amniotic infection most cells in the exudate are maternal. These leucocytes participate in antibacterial defence of the amniotic cavity in conjunction with substances such as zinc polypeptide and lysozyme and may contribute directly to fetal defence. Immunoglobulins may be produced in the cord of placenta only in protracted lesions such as 'healed' funisitis. Individual variations in the resistance of the membranes to bacterial penetration are possible. In viral infections a massive multifocal production by plasmacytes of immunoglobulins M, G and A is seen in affected villi. The secretion of non-specific antiviral substances in the infected placenta is possible. In all affected villi there is an activation of fixed macrophages (Hofbauer cells) that remain partly 'immature', i.e. are lysozyme-negative. Multifocal lymphoplasmacytic villitis is uncommon and has helped to focus the diagnosis on prenatal infection. In contrast, non-specific lymphocytic villitis is common; since there is no morphological difference between cases known to be associated with an infection, e.g. varicella, and the others, many cases may well be due to silent infection, although a graft-versus-host reactions remains a distinct possibility.

Amnion

Impact of Maternal Aspirin Therapy on Neonatal Epigenetic Patterns.

BACKGROUND: Low-dose aspirin (LDA) is an intervention recommended to prevent the development of hypertensive disorders of pregnancy (HDP) in high-risk pregnancies. Maternal conditions such as HDP have been associated with cord blood epigenetic changes including those related to cardiovascular processes; however, it is unclear whether maternal aspirin therapy may impact neonatal epigenetics in otherwise healthy high-risk pregnancy. OBJECTIVE: This study aimed to determine if maternal LDA exposure in utero leads to altered DNA methylation in umbilical cord blood cells in term neonates compared with controls not exposed to aspirin, and to identify if these methylation changes alter key pathways in the development of chronic disease. METHODS: Umbilical cord blood was collected from 10 neonates without LDA exposure and 13 neonates with LDA exposure in utero. Patients with hypertensive disorders of pregnancy, COVID-19, and chorioamnionitis were excluded. Genomic DNA was isolated from umbilical cord blood cells and genome-wide DNA methylation was performed using Illumina Methylation EPIC assay. RESULTS: A total of 155 differentially methylated loci (81 genes were hypermethylated and 74 were hypomethylated) were identified in LDA-exposed neonatal umbilical cord blood compared with the control group. Important canonical pathways identified by Ingenuity Pathway Analysis (IPA) were related to Th1 and Th2 signaling and classical (M1) macrophage activation. The genes affected by LDA exposure were associated with cardiac and renal systems. CONCLUSION: LDA exposure led to differential DNA methylation in umbilical cord blood. The differentially methylated genes were related to inflammatory pathways as well as cardiac and renal toxicity pathways. LDA exposure in utero may promote altered health programming in the neonate in areas impacting cardiovascular health. KEY POINTS: · Maternal aspirin exposure is associated with differential DNA methylation in cord blood.. · Cord blood epigenetic changes associated with maternal aspirin relate to anti-inflammatory pathways.. · Research on potential protective impact of maternal aspirin on neonatal epigenetics is warranted..

Humans

Intrauterine infections in nonhuman primates.

Gross and histologic examination of five nonhuman primate placentas revealed inflammatory processes, either of the ascending type, with chorioamnionitis and fetal vasculitis, or of the hematogenous type with villitis. These reactions were similar to those occurring in man, with known implications for perinatal outcome.

Animals

Unexpected disseminated herpes simplex infection in a newborn.

Disseminated herpes simplex virus type 2 was unexpectedly discovered in a baby delivered by primary cesarean section at 36 weeks' gestation prior to rupture of the membranes. The mother was free of orogenital lesions at each prenatal examination. Examination of the placenta revealed chorioamnionitis implicating an ascending infection from the mother's infected genital tract.

Adult

Pathogenicity of ureaplasmas for animals and man.

Since their original isolation from the genital tract of man, ureaplasmas, previously termed T-strain mycoplasmas, have been isolated from a variety of animal species. Under experimental conditions they have been shown to cause mastitis in cattle, goats and mice, and observations made on naturally-occurring bovine pneumonia, as well as the results of experimental inoculation, suggest that ureaplasmas are responsible for a portion of bovine cuffing pneumonia. Ureaplasmas have been isolated from the genital tract of a wide variety of animals and have the potential for causing disease in this anatomical area, as the results of experimental intra-urethral inoculation of goats, for example, indicate. However, there are no data, as yet, to incriminate ureaplasmas as a cause of naturally-occurring genital tract disease nor as a cause of infertility, the latter being an area in which the results of studies are often conflicting and difficult to interpret. In man, the rôle of ureaplasmas in genito-urinary disease has been a bone of contention for many years. Experimentally, ureaplasmas produce bladder calculi in rats but so far there is no evidence that they do so in man. Further, there are no convincing data to support the notion that infertile couples possessing ureaplasmas should be treated with tetracyclines. There is an undoubted association between spontaneous abortion and low birth-weight on the one hand and the presence of ureaplasmas in the mother, abortus or infant on the other. However, evidence that the organisms cause abortion is lacking and whether they are directly responsible for low birth-weight is unknown. The association between chorioamnionitis and ureaplasma isolation is provocative enough to stimulate further work. In the case of non-gonococcal urethritis, the weight of evidence suggests that ureaplasmas cause the disease in some men. This is based on quantitative isolation, volunteer inoculation, as well as treatment studies including the use of antibiotics, such as rifampicin, which differentiate between chlamydiae and ureaplasmas.

Animals

Intra-amniotic infection: diagnosis, nomenclature, clinical significance, management, and microbiologic tools used for the diagnosis.

SUMMARYIntra-amniotic infection is the main cause of spontaneous preterm birth and adverse maternal-fetal outcomes; therefore, rapid, robust, and accurate diagnosis remains a clinical priority. Conventional microbiological techniques, especially culture-based methods, are limited by long turnaround times and the inability to detect fastidious or unculturable organisms. This review summarizes the diagnosis, nomenclature, clinical significance, management, and laboratory approaches for diagnosing intra-amniotic infection. Targeted nucleic acid amplification methods, including species-specific polymerase chain reaction and broad-range 16S rRNA gene sequencing, have improved the detection of bacterial DNA and enabled the identification of organisms that evade routine culture in intra-amniotic infection. More recently, whole-genome sequencing and metagenomic next-generation sequencing have provided culture-independent strategies for comprehensive pathogen profiling, allowing simultaneous detection of bacteria, viruses, and fungi, as well as characterization of antimicrobial resistance determinants and virulence-associated genes. However, challenges remain, particularly in low-biomass samples such as amniotic fluid, where contamination, host DNA background, and data interpretation can compromise specificity. This review critically evaluates the advantages and limitations of each molecular modality and discusses pre-analytical, analytical, and bioinformatic considerations essential for reliable implementation. Integration of molecular diagnostics into clinical workflows holds promise for improving etiological diagnosis and guiding targeted therapy in intra-amniotic infection, thereby improving maternal and fetal outcomes.

Humans