ArticleInfection and immunity2004
Interleukin-18 is an essential element in host resistance to experimental group B streptococcal disease in neonates.
Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- Neurodevelopmental impairment associated with neonatal invasive group BBrain, behavior, & immunity - health · 2024Article
- Constitutive secretion of pro-IL-18 allows keratinocytes to initiate inflammation during bacterial infection.PLoS pathogens · 2023Article
- IL-18 Signaling Is Essential for Causing Streptococcal Toxic Shock-like Syndrome (STSLS).Life (Basel, Switzerland) · 2022Article
- CodY Is a Global Transcriptional Regulator Required for Virulence in Group BFrontiers in microbiology · 2022Article
- Protective role of IL-18 in host defenses against group B Streptococcus.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2021Article
- Group B Streptococcal Maternal Colonization and Neonatal Disease: Molecular Mechanisms and Preventative Approaches.Frontiers in pediatrics · 2018Review
- Natural Killer Cell Functions during the Innate Immune Response to Pathogenic Streptococci.Frontiers in microbiology · 2017Article
- Neonatal Group B Streptococcal Disease in Otherwise Healthy Infants: Failure of Specific Neonatal Immune Responses.Frontiers in immunology · 2017Article
- 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
- Inflammasome/IL-1β Responses to Streptococcal Pathogens.Frontiers in immunology · 2015Review
- Essential role of interleukin-1 signaling in host defenses against group B streptococcus.mBio · 2014Article
- Activation of the NLRP3 inflammasome by group B streptococci.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Biomarker discovery and development in pediatric critical care medicine.Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies · 2011Review
- Role of the inflammasome, IL-1β, and IL-18 in bacterial infections.TheScientificWorldJournal · 2011Review
- Pathophysiology and treatment of septic shock in neonates.Clinics in perinatology · 2010Review
- TLR-independent type I interferon induction in response to an extracellular bacterial pathogen via intracellular recognition of its DNA.Cell host & microbe · 2008Article
- Induction and termination of inflammatory signaling in group B streptococcal sepsis.Immunological reviews · 2008Review
- Identification of diagnostic biomarkers for infection in premature neonates.Molecular & cellular proteomics : MCP · 2008Article
- Bacteroides fragilis-derived lipopolysaccharide produces cell activation and lethal toxicity via toll-like receptor 4.Infection and immunity · 2005Article
- Use of biomarkers in pediatric sepsis: literature review.Revista Brasileira de terapia intensivaReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies demonstrated that interleukin-12 (IL-12)-dependent gamma interferon (IFN-gamma) responses have a major role in restricting in vivo bacterial growth during infection of mice with group B streptococci (GBS), important human pathogens. Like IL-12, IL-18 is a potent IFN-gamma inducer. The role of IL-18 in experimental GBS infection was investigated here. Significant elevations of IL-18 levels over baseline values were detected in plasma samples from neonatal mice rendered septic with GBS. Neutralization of IL-18 significantly increased mortality and bacterial burden (P < 0.05). In contrast, administration of recombinant IL-18 (rIL-18) before or after GBS challenge remarkably improved survival and decreased blood colony counts, in association with increased IFN-gamma production by spleen cells. The beneficial effects of rIL-18 were counteracted by administration of neutralizing anti-IFN-gamma monoclonal antibodies, indicating that the effects of IL-18 were mediated by IFN-gamma. Finally, low rIL-18 doses that had no effect of their own on bacterial burden could act in synergy with rIL-12 to protect neonatal mice during GBS infection. Collectively, our data indicate that IL-18 responses have an important role in host defenses against GBS and that rIL-18 may be useful in alternative strategies to treat neonatal GBS disease.
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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.