Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (738 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Inflammation of the placental membranes (chorion; amnion) and connected tissues such as fetal blood vessels and umbilical cord. It is often associated with intrauterine ascending infections during pregnancy.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Chorioamnionitides; Amnionitis; Amnionitides; Funisitis; Funisitides.
Where it fits in the MeSH classification
- Broader topics
- Fetal Diseases; Premature Rupture of Fetal Membranes; Placenta Diseases
Related concepts
- Inflammation
- Chorion
- Amnion
- Blood Vessels
- Umbilical Cord
- Pregnancy
Research landscape
PubMed indexes 3,921 records tagged with the MeSH heading “Chorioamnionitis” (counts retrieved 2026-11-04). 921 of them (23.5%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 1,327 records.
Reviews account for 534 records (13.6%) and meta-analyses for 84. Randomized controlled trials number 120 (3.1%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 844 |
| 2000-2009 | 829 |
| 2010-2019 | 1,327 |
| 2020 onward | 921 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 534 | 13.6% |
| Meta-analyses | 84 | 2.1% |
| Randomized controlled trials | 120 | 3.1% |
Method: PubMed query "Chorioamnionitis"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in kidney, urology and women's health
Kidney, urinary and reproductive health research uses lab markers (such as creatinine), imaging, symptom scores and registry data on pregnancy and birth. Findings about pregnancy are especially sensitive to who was studied and when in pregnancy exposure occurred. Nothing on this page is advice about treatment, fertility or pregnancy; speak to a qualified clinician. Check the population, the outcome measured and whether the study accounted for other health differences between groups.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Preterm birth and sustained inflammation: consequences for the neonate | 2020 | Review article Design not recorded in structured metadata | 248 | cc by PMID 32661735 · DOI · PMC7508934 |
| The Airway Microbiome at Birth | 2016 | Research article Design not recorded in structured metadata | 154 | cc by PMID 27488092 · DOI · PMC4973241 |
| Preterm Brain Injury, Antenatal Triggers, and Therapeutics: Timing Is Key | 2020 | Review article Design not recorded in structured metadata | 96 | cc by PMID 32785181 · DOI · PMC7464163 |
| Prenatal inflammation impairs early CD11c-positive microglia induction and delays myelination in neurodevelopmental disorders | 2025 | Research article Design not recorded in structured metadata | 10 | cc by PMID 39824932 · DOI · PMC11742679 |
Preterm birth and sustained inflammation: consequences for the neonate [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Almost half of all preterm births are caused or triggered by an inflammatory process at the feto-maternal interface resulting in preterm labor or rupture of membranes with or without chorioamnionitis ("first inflammatory hit").
- Closing excerpt
- This review will outline the (i) role of inflammation for short-term consequences of preterm birth and (ii) the effect of SI on organ development and long-term outcome.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (206 words)
Almost half of all preterm births are caused or triggered by an inflammatory process at the feto-maternal interface resulting in preterm labor or rupture of membranes with or without chorioamnionitis ("first inflammatory hit"). Preterm babies have highly vulnerable body surfaces and immature organ systems. They are postnatally confronted with a drastically altered antigen exposure including hospital-specific microbes, artificial devices, drugs, nutritional antigens, and hypoxia or hyperoxia ("second inflammatory hit"). This is of particular importance to extremely preterm infants born before 28 weeks, as they have not experienced important "third-trimester" adaptation processes to tolerate maternal and self-antigens. Instead of a balanced adaptation to extrauterine life, the delicate co-regulation between immune defense mechanisms and immunosuppression (tolerance) to allow microbiome establishment is therefore often disturbed. Hence, preterm infants are predisposed to sepsis but also to several injurious conditions that can contribute to the onset or perpetuation of sustained inflammation (SI). This is a continuing challenge to clinicians involved in the care of preterm infants, as SI is regarded as a crucial mediator for mortality and the development of morbidities in preterm infants. This review will outline the (i) role of inflammation for short-term consequences of preterm birth and (ii) the effect of SI on organ development and long-term outcome.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32661735 · DOI · PMC7508934
The Airway Microbiome at Birth [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Alterations of pulmonary microbiome have been recognized in multiple respiratory disorders.
- Closing excerpt
- We speculate that the early airway microbiome may prime the developing pulmonary immune system, and dysbiosis in its development may set the stage for subsequent lung disease.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (163 words)
Alterations of pulmonary microbiome have been recognized in multiple respiratory disorders. It is critically important to ascertain if an airway microbiome exists at birth and if so, whether it is associated with subsequent lung disease. We found an established diverse and similar airway microbiome at birth in both preterm and term infants, which was more diverse and different from that of older preterm infants with established chronic lung disease (bronchopulmonary dysplasia). Consistent temporal dysbiotic changes in the airway microbiome were seen from birth to the development of bronchopulmonary dysplasia in extremely preterm infants. Genus Lactobacillus was decreased at birth in infants with chorioamnionitis and in preterm infants who subsequently went on to develop lung disease. Our results, taken together with previous literature indicating a placental and amniotic fluid microbiome, suggest fetal acquisition of an airway microbiome. We speculate that the early airway microbiome may prime the developing pulmonary immune system, and dysbiosis in its development may set the stage for subsequent lung disease.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 27488092 · DOI · PMC4973241
Preterm Brain Injury, Antenatal Triggers, and Therapeutics: Timing Is Key [3]
Abstract reading summary — source excerpts
- Opening excerpt
- With a worldwide incidence of 15 million cases, preterm birth is a major contributor to neonatal mortality and morbidity, and concomitant social and economic burden Preterm infants are predisposed to life-long neurological disorders due to the immaturity of the brain.
- Closing excerpt
- This review focuses on chorioamnionitis and hypoxia-ischemia, which are two important antenatal risk factors for preterm brain injury, and highlights the latest insights on its pathophysiology, potential treatment, and future perspectives to narrow the translational gap between preclinical research and clinical applications.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (173 words)
With a worldwide incidence of 15 million cases, preterm birth is a major contributor to neonatal mortality and morbidity, and concomitant social and economic burden Preterm infants are predisposed to life-long neurological disorders due to the immaturity of the brain. The risks are inversely proportional to maturity at birth. In the majority of extremely preterm infants (<28 weeks' gestation), perinatal brain injury is associated with exposure to multiple inflammatory perinatal triggers that include antenatal infection (i.e., chorioamnionitis), hypoxia-ischemia, and various postnatal injurious triggers (i.e., oxidative stress, sepsis, mechanical ventilation, hemodynamic instability). These perinatal insults cause a self-perpetuating cascade of peripheral and cerebral inflammation that plays a critical role in the etiology of diffuse white and grey matter injuries that underlies a spectrum of connectivity deficits in survivors from extremely preterm birth. This review focuses on chorioamnionitis and hypoxia-ischemia, which are two important antenatal risk factors for preterm brain injury, and highlights the latest insights on its pathophysiology, potential treatment, and future perspectives to narrow the translational gap between preclinical research and clinical applications.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32785181 · DOI · PMC7464163
Prenatal inflammation impairs early CD11c-positive microglia induction and delays myelination in neurodevelopmental disorders [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Histological chorioamnionitis (HCA) is a form of maternal immune activation (MIA) linked to an increased risk of neurodevelopmental disorders in offspring.
- Closing excerpt
- Our findings may inform strategies for improving outcomes in infants with HCA.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (196 words)
Histological chorioamnionitis (HCA) is a form of maternal immune activation (MIA) linked to an increased risk of neurodevelopmental disorders in offspring. Our previous study identified neurodevelopmental impairments in an MIA mouse model mimicking HCA. Thus, this study investigated the role of CD11c+ microglia, key contributors to myelination through IGF-1 production, in this pathology. In the mouse model, the CD11c+ microglial population was significantly lower in the MIA group than in the control group on postnatal day 3 (PN3d). Furthermore, myelination-related protein levels significantly decreased in the MIA group at PN8d. In humans, preterm infants with HCA exhibited higher IL-6 and IL-17A cord-serum levels and lower IGF-1 levels than those without HCA, followed by a higher incidence of delayed myelination on magnetic resonance imaging at the term-equivalent age. In silico analysis revealed that the transient induction of CD11c+ microglia during early development occurred similarly in mice and humans. Notably, a lack of high CD11c+ microglial population has been observed in children with neurodevelopmental disorders. This study reports impaired induction of CD11c+ microglia during postnatal development in a mouse model of MIA associated with delayed myelination. Our findings may inform strategies for improving outcomes in infants with HCA.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39824932 · DOI · PMC11742679
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Acute chorioamnionitis and funisitis: definition, pathologic features, and clinical significance [5]
- Research article Chorioamnionitis as a risk factor for cerebral palsy: A meta-analysis [6]
- Research article Diagnosis and management of clinical chorioamnionitis [7]
- Research article Chronic inflammation of the placenta: definition, classification, pathogenesis, and clinical significance [8]
- Research article Committee Opinion No. 712: Intrapartum Management of Intraamniotic Infection [9]
- Research article Premature labor and intra-amniotic infection. Clinical aspects and role of the cytokines in diagnosis and pathophysiology [10]
References
- Humberg A, Fortmann I, Siller B, Kopp MV, Herting E, Göpel W, et al.. Preterm birth and sustained inflammation: consequences for the neonate. . 2020. PMID 32661735 · DOI · PMC7508934
- Lal CV, Travers C, Aghai ZH, Eipers P, Jilling T, Halloran B, et al.. The Airway Microbiome at Birth. . 2016. PMID 27488092 · DOI · PMC4973241
- Ophelders DRMG, Gussenhoven R, Klein L, Jellema RK, Westerlaken RJJ, Hütten MC, et al.. Preterm Brain Injury, Antenatal Triggers, and Therapeutics: Timing Is Key. . 2020. PMID 32785181 · DOI · PMC7464163
- Fuma K, Iitani Y, Imai K, Ushida T, Tano S, Yoshida K, et al.. Prenatal inflammation impairs early CD11c-positive microglia induction and delays myelination in neurodevelopmental disorders. . 2025. PMID 39824932 · DOI · PMC11742679
- Kim CJ, Romero R, Chaemsaithong P, Chaemsaithong P, Chaiyasit N, Yoon BH, et al.. Acute chorioamnionitis and funisitis: definition, pathologic features, and clinical significance. Am J Obstet Gynecol. 2015. PMID 26428501 · DOI · PMC4774647
- Wu YW, Colford JM. Chorioamnionitis as a risk factor for cerebral palsy: A meta-analysis. JAMA. 2000. PMID 10989405 · DOI
- Tita AT, Andrews WW. Diagnosis and management of clinical chorioamnionitis. Clin Perinatol. 2010. PMID 20569811 · DOI · PMC3008318
- Kim CJ, Romero R, Chaemsaithong P, Chaemsaithong P, Kim JS. Chronic inflammation of the placenta: definition, classification, pathogenesis, and clinical significance. Am J Obstet Gynecol. 2015. PMID 26428503 · DOI · PMC4782598
- . Committee Opinion No. 712: Intrapartum Management of Intraamniotic Infection. Obstet Gynecol. 2017. PMID 28742677 · DOI
- Gomez R, Ghezzi F, Romero R, Muñoz H, Tolosa JE, Rojas I. Premature labor and intra-amniotic infection. Clinical aspects and role of the cytokines in diagnosis and pathophysiology. Clin Perinatol. 1995. PMID 7671540 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.