ArticleImmunology2014
Lack of formyl peptide receptor 1 and 2 leads to more severe inflammation and higher mortality in mice with of pneumococcal meningitis.
Article in Immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 59 citations in OpenAlex.
- Genetic deletion of Alx/Fpr2 differentially regulates pulmonary inflammation in the absence and presence of acute lung injury.ImmunoHorizons · 2025Article
- Focusing on Formyl Peptide Receptors after Traumatic Spinal Cord Injury: from Immune Response to Neurogenesis.Neurochemical research · 2025Review
- Article
- Lipoxin ACardiovascular diabetology · 2024Article
- Differential requirement of formyl peptide receptor 1 in macrophages and neutrophils in the host defense against Mycobacterium tuberculosis Infection.Scientific reports · 2024Article
- Differential requirement of Formyl Peptide Receptor 1 in macrophages and neutrophils in the host defense againstResearch square · 2024Article
- Mind the Gap-A Perspective on Strategies for Protecting against Bacterial Infections during the Period from Infection to Eradication.Microorganisms · 2023Review
- Developmental and homeostatic signaling transmitted by the G-protein coupled receptor FPR2.International immunopharmacology · 2023Review
- Article
- Formyl peptide receptor 2 is an emerging modulator of inflammation in the liver.Experimental & molecular medicine · 2023Review
- Formyl peptide receptor-1 (FPR1) represses intestinal oncogenesis.Oncoimmunology · 2023Article
- Rs867228 in FPR1 accelerates the manifestation of luminal B breast cancer.Oncoimmunology · 2023Article
- Fpr2 exacerbatesFrontiers in immunology · 2023Article
- Promiscuous Receptors and Neuroinflammation: The Formyl Peptide Class.Life (Basel, Switzerland) · 2022Review
- Formylpeptide receptor 2: Nomenclature, structure, signalling and translational perspectives: IUPHAR review 35.British journal of pharmacology · 2022Review
- Neuroprotective effects of CysLTR antagonist onExperimental and therapeutic medicine · 2022Article
- CCL2 Inhibition of Pro-Resolving Mediators Potentiates Neuroinflammation in Astrocytes.International journal of molecular sciences · 2022Article
- Immune Memory After Respiratory Infection WithFrontiers in cellular and infection microbiology · 2022Article
- The N-Formyl Peptide Receptor 2 (FPR2) Agonist MR-39 Improves Ex Vivo and In Vivo Amyloid Beta (1-42)-Induced Neuroinflammation in Mouse Models of Alzheimer's Disease.Molecular neurobiology · 2021Article
- Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Bacterial meningitis is, despite progress in research and the development of new treatment strategies, still a cause of severe neuronal sequelae. The brain is protected from penetrating pathogens by both the blood-brain barrier and the innate immune system. The invading pathogens are recognized by pattern recognition receptors including the G-protein coupled formyl peptide receptors (FPRs), which are expressed by immune cells of the central nervous system. The expression of FPRs is up-regulated during bacterial meningitis, but the consequence on the progression of inflammation and impact on mortality are far from clear. Therefore, we used mFPR1 and mFPR2-deficient mice to investigate the effects on inflammation, bacterial growth and mortality in a mouse model of pneumococcal meningitis. Our results revealed increased bacterial burden, increased neutrophil infiltration and higher mortality in mFPR1/2-deficient mice in comparison to wild-type mice. The mFPR1- or mFPR2-deficient mice also showed significantly increased glial cell density, whereas the immune responses including the expression of anti-inflammatory cytokines and antimicrobial peptides were decreased in bacterial meningitis. Taken together, the results suggest that FPR1 and FPR2 play an important role in the innate immune responses against Streptococcus pneumoniae within the central nervous system and the lack of the receptors leads to a dysregulation of the inflammatory response compared with wild-type mice.
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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.