ArticleScientific reports2019
Sex-specific maternofetal innate immune responses triggered by group B Streptococci.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- Urogenital immune signatures are associated with birth outcomes after maternal urinary tract infection.Science translational medicine · 2026Article
- Sex-specific outcomes following chorioamnionitis.Pediatric research · 2026Review
- A mother's touch: microbial guardians of early immune imprinting.Trends in immunology · 2026Review
- Single-cell analysis of the decidua unveils the mechanism of anti-inflammatory exosomes for chorioamnionitis in nonhuman primates.Science advances · 2025Article
- Defining knowledge gaps in preterm birth research: Can biomarkers fill the gaps?Frontiers in medicine · 2025Review
- Immune Alterations in the Intrauterine Environment Shape Offspring Brain Development in a Sex-Specific Manner.Biological psychiatry · 2025Review
- Distinct maternofetal immune signatures delineate preterm birth onset following urinary tract infection.bioRxiv : the preprint server for biology · 2024Article
- IL-1 Blockade Mitigates Autism and Cerebral Palsy Traits in Offspring In-Utero Exposed to Group BInternational journal of molecular sciences · 2024Article
- Neurodevelopmental impairment associated with neonatal invasive group BBrain, behavior, & immunity - health · 2024Article
- The Autism Spectrum Disorder and Its Possible Origins in Pregnancy.International journal of environmental research and public health · 2024Review
- Gestational diabetes augments group B Streptococcus infection by disrupting maternal immunity and the vaginal microbiota.Nature communications · 2024Article
- Brain growth until adolescence after a neonatal focal injury: sex related differences beyond lesion effect.Frontiers in neuroscience · 2024Article
- Impact of sex, race, and social determinants of health on neonatal outcomes.Frontiers in pediatrics · 2024Review
- Maternal Group B Streptococcus Infection Correlates Inversely With Preeclampsia in Pregnant African American Women.Maternal-fetal medicine (Wolters Kluwer Health, Inc.) · 2024Article
- Sex-Specific Dysconnective Brain Injuries and Neuropsychiatric Conditions such as Autism Spectrum Disorder Caused by Group BInternational journal of molecular sciences · 2023Review
- Conventional electroencephalography for accurate assessment of brain maturation in preterm infants following perinatal inflammation.Pediatric research · 2023Article
- Placental macrophage responses to viral and bacterial ligands and the influence of fetal sex.iScience · 2022Article
- Necroptosis Blockade Potentiates the Neuroprotective Effect of Hypothermia in Neonatal Hypoxic-Ischemic Encephalopathy.Biomedicines · 2022Article
- Mast cell-derived factor XIIIA contributes to sexual dimorphic defense against group B streptococcal infections.The Journal of clinical investigation · 2022Article
- Androgens Upregulate Pathogen-Induced Placental Innate Immune Response.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Group B Streptococcus (GBS) is one of the most common bacteria isolated in human chorioamnionitis, which is a major risk factor for premature birth and brain injuries. Males are at greater risk than females for developing lifelong neurobehavioural disorders, although the origins of this sex bias remain poorly understood. We previously showed that end-gestational inflammation triggered by GBS led to early neurodevelopmental impairments mainly in the male rat progeny. Identifying key inflammatory players involved in maternofetal immune activation by specific pathogens is critical to develop appropriate novel therapeutic interventions. We aimed to map out the GBS-induced profile of innate immune biomarkers in the maternal-placental-fetal axis, and to compare this immune profile between male and female tissues. We describe here that the GBS-induced immune signalling involved significantly higher levels of interleukin (IL)-1β, cytokine-induced neutrophil chemoattractant-1 (CINC-1/CXCL1) and polymorphonuclear cells (PMNs) infiltration in male compared to female maternofetal tissues. Although male - but not female - fetuses presented increased levels of IL-1β, fetuses from both sexes in-utero exposed to GBS had increased levels of TNF-α in their circulation. Levels of IL-1β detected in fetal sera correlated positively with the levels found in maternal circulation. Here, we report for the first time that the maternofetal innate immune signalling induced by GBS presents a sexually dichotomous profile, with more prominent inflammation in males than females. These sex-specific placental and fetal pro-inflammatory responses are in keeping with the higher susceptibility of the male population for preterm birth, brain injuries and neurodevelopmental disorders such as cerebral palsy and autism spectrum disorders.
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