ArticleInfection and immunity2014
The interleukin-1β/CXCL1/2/neutrophil axis mediates host protection against group B streptococcal infection.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.
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Who cites it
78 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.
- Immunopathological Changes in SARS-CoV-2 Critical and Non-critical Pneumonia Patients: A Systematic Review to Determine the Cause of Co-infection.Frontiers in public health · 2020Pooled it
- Review
- Dietary omega-6 arachidonic acid and omega-3 docosahexaenoic acid supplementation differentially impact skeletal muscle inflammaging in mice.bioRxiv : the preprint server for biology · 2026Article
- The role of persistent inflammation in failed recovery after perinatal brain injury: is resolution the cure?Journal of neuroinflammation · 2026Review
- Human neutrophils recognize group B streptococciFrontiers in immunology · 2026Article
- Characterization of Cytokine Treatment on Human Pancreatic Islets by Top-Down Proteomics.Proteomics · 2025Article
- Neutrophils at the Maternal-Fetal Interface: Agents of Protection or Destruction?American journal of reproductive immunology (New York, N.Y. : 1989) · 2025Review
- Bone marrow neutrophil density regulates myelopoiesis during obesity and weight loss.The Journal of experimental medicine · 2025Article
- IL-33-primed NLRP3 inflammasome in basophils drives IL-1β production and initiates atopic dermatitis inflammation.Cell death discovery · 2025Article
- Characterization of cytokine treatment on human pancreatic islets by top-down proteomics.bioRxiv : the preprint server for biology · 2025Article
- Group B streptococcal infections in pregnancy and early life.Clinical microbiology reviews · 2025Review
- Group B Streptococcal Membrane Vesicles Induce Proinflammatory Cytokine Production and Are Sensed in an NLRP3 Inflammasome-Dependent Mechanism in a Human Macrophage-like Cell Line.ACS infectious diseases · 2025Article
- Immunogenicity of culture filtrated proteins and whole-cell killed formalin ofOpen veterinary journal · 2024Article
- Unveiling the crucial role of ferroptosis in host resistance to streptococcus agalactiae infection.Cell death discovery · 2024Article
- Preliminary study of BF/C2 on immune mechanism of grass carp against GCRV infection.BMC genomics · 2024Article
- Transcriptional profiling links unique human macrophage phenotypes to the growth of intracellular Salmonella enterica serovar Typhi.Scientific reports · 2024Article
- Impaired autophagy in myeloid cells aggravates psoriasis-like skin inflammation through the IL-1β/CXCL2/neutrophil axis.Cell & bioscience · 2024Article
- Structural properties of immune complexes formed by viral antigens and specific antibodies shape the inflammatory response of macrophages.Cell & bioscience · 2024Article
- Salmonella spvC gene suppresses macrophage/neutrophil antibacterial defense mediated by gasdermin D.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Radiation-Induced Innate Neutrophil Response in Tumor Is Mediated by the CXCLs/CXCR2 Axis.Cancers · 2023Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have indicated that group B streptococcus (GBS), a frequent human pathogen, potently induces the release of interleukin-1β (IL-1β), an important mediator of inflammatory responses. Since little is known about the role of this cytokine in GBS disease, we analyzed the outcome of infection in IL-1β-deficient mice. These animals were markedly sensitive to GBS infection, with most of them dying under challenge conditions that caused no deaths in wild-type control mice. Lethality was due to the inability of the IL-1β-deficient mice to control local GBS replication and dissemination to target organs, such as the brain and the kidneys. Moreover, in a model of inflammation induced by the intraperitoneal injection of killed GBS, a lack of IL-1β was associated with selective impairment in the production of the neutrophil chemokines CXCL1 and CXCL2 and in neutrophil recruitment to the peritoneal cavity. Decreased blood neutrophil counts and impaired neutrophil recruitment to the brain and kidneys were also observed during GBS infection in IL-1β-deficient mice concomitantly with a reduction in CXCL1 and CXCL2 tissue levels. Notably, the hypersusceptibility to GBS infection observed in the immune-deficient animals was recapitulated by neutrophil depletion with anti-Gr1 antibodies. Collectively, our data identify a cytokine circuit that involves IL-1β-induced production of CXCL1 and CXCL2 and leads the recruitment of neutrophils to GBS infection sites. Moreover, our data point to an essential role of these cells in controlling the progression and outcome of GBS disease.
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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.