Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Induction and termination of inflammatory signaling in group B streptococcal sepsis

19 Sept 2008

Abstract excerpt

SUMMARY: Group 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...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Immune Response and Inflammation
Share to Neonatal and Maternal Infections
Share to Sepsis Diagnosis and Treatment

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 18837779
DOI: 10.1111/j.1600-065x.2008.00673.x

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Induction and termination of inflammatory signaling in group B streptococcal sepsisPMID 18837779Read ↗

A Mechanism for Neurodegeneration Induced by Group B Streptococci through Activation of the TLR2/MyD88 Pathway in MicrogliaSemantic proximity Read ↗

TLR2 and Caspase-8 Are Essential for Group B <i>Streptococcus</i> -Induced Apoptosis in MicrogliaSemantic proximity Read ↗

Interaction of Streptococcus agalactiae and Cellular Innate Immunity in Colonization and DiseaseSemantic proximity Read ↗

Bacterial Sensing, Cell Signaling, and Modulation of the Immune Response During SepsisSemantic proximity Read ↗

An impaired inflammatory cytokine response to gram-negative LPS in human neonates is associated with the defective TLR-mediated signaling pathway.Semantic proximity Read ↗

Responses of innate immune cells to group A StreptococcusSemantic proximity Read ↗

Toll-like receptor signaling in sepsisSemantic proximity Read ↗

Codevelopment of Microbiota and Innate Immunity and the Risk for Group B Streptococcal DiseaseSemantic proximity Read ↗

Dual role of TLR2 and myeloid differentiation factor 88 in a mouse model of invasive group B streptococcal disease.Semantic proximity Read ↗

Toll-like receptor 2 is partially involved in the activation of murine astrocytes by Streptococcus suis, an important zoonotic agent of meningitis.Semantic proximity Read ↗

Group A Streptococcus Activates Type I Interferon Production and MyD88-dependent Signaling without Involvement of TLR2, TLR4, and TLR9Semantic proximity Read ↗

Leukotriene B4 enhances innate immune defense against the puerperal sepsis agent Streptococcus pyogenes.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.