ReviewImmunological reviews2008
Induction and termination of inflammatory signaling in group B streptococcal sepsis.
Review in Immunological reviews, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- The Key Drivers of Brain Injury by Systemic Inflammatory Responses after Sepsis: Microglia and Neuroinflammation.Molecular neurobiology · 2023Pooled it
- Shared immune biomarkers in necrotizing enterocolitis and neonatal sepsis identified via bioinformatics and machine learning.Scientific reports · 2025Article
- Inhibition of Farnesoid-x-receptor signaling during abdominal sepsis by dysbiosis exacerbates gut barrier dysfunction.Cell communication and signaling : CCS · 2025Article
- Sex-Specific Dysconnective Brain Injuries and Neuropsychiatric Conditions such as Autism Spectrum Disorder Caused by Group BInternational journal of molecular sciences · 2023Review
- Expression of immune checkpoint molecules on adult and neonatal T-cells.Immunologic research · 2023Article
- Group BScience advances · 2022Article
- Article
- Distinct Group BInfection and immunity · 2021Article
- Streptococcus agalactiae in pregnant women: serotype and antimicrobial susceptibility patterns over five years in Eastern Sicily (Italy).European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2020Article
- Progressive Control of Streptococcus agalactiae-Induced Innate Inflammatory Response Is Associated with Time Course Expression of MicroRNA-223 by Neutrophils.Infection and immunity · 2020Article
- Article
- Lactobacillus strains vary in their ability to interact with human endometrial stromal cells.PloS one · 2020Article
- Modulation of Death and Inflammatory Signaling in Decidual Stromal Cells following Exposure to Group BInfection and immunity · 2019Article
- Sex-specific maternofetal innate immune responses triggered by group B Streptococci.Scientific reports · 2019Article
- Genetically distinct Group B Streptococcus strains induce varying macrophage cytokine responses.PloS one · 2019Article
- Neonatal neutrophils stimulated by group B Streptococcus induce a proinflammatory T-helper cell bias.Pediatric research · 2018Article
- Natural Killer Cell Functions during the Innate Immune Response to Pathogenic Streptococci.Frontiers in microbiology · 2017Article
- Genomic Recombination Leading to Decreased Virulence of Group B Streptococcus in a Mouse Model of Adult Invasive Disease.Pathogens (Basel, Switzerland) · 2016Article
- High expression levels of macrophage migration inhibitory factor sustain the innate immune responses of neonates.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Group B Streptococcus Induces a Robust IFN-γ Response by CD4(+) T Cells in an In Vitro and In Vivo Model.Journal of immunology research · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
summaryGroup B streptococcus (GBS) is part of the normal genital and gastrointestinal flora in healthy humans. However, GBS is a major cause of sepsis and meningitis in newborn infants in the Western world and an important pathogen in many developing countries. The dissection of the host response to GBS may increase the general understanding of innate immunity in sepsis, because newborn infants lack a sufficient adaptive response. Inflammatory signal induction in macrophages by GBS seems largely preserved in newborn infants, as shown both in vitro and in vivo. The engagement of Toll-like receptor 2 (TLR2) by lipoproteins and a myeloid differentiation factor 88 (MyD88)--dependent pathway induced by GBS cell wall are both important in this context. TLR2 activation of microglia by GBS induces neuronal damage, which might account for the high morbidity of GBS meningitis. At the same time, TLR2 mediates activation-induced cell death (AICD), a process involved in the containment of inflammation. In newborn infants, AICD and anti-bacterial polymorphonuclear leukocyte activity appears to be compromised. Accordingly, neonatal aberrations in the pathogen-specific negative control of inflammatory signaling are likely to contribute to excessive inflammation and neurological sequelae in GBS sepsis and meningitis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.