ArticleJournal of immunology (Baltimore, Md. : 1950)2014
The receptor for the complement C3a anaphylatoxin (C3aR) provides host protection against Listeria monocytogenes-induced apoptosis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- The Role of the C3a-C3aR Pathway in Diseases: Latest Research Advances.Mediators of inflammation · 2026Review
- Advances in mechanism and regulation of PANoptosis: Prospects in disease treatment.Frontiers in immunology · 2023Review
- Streptococcus suis Serotype 2 Infection Induces Splenomegaly with Splenocyte Apoptosis.Microbiology spectrum · 2022Article
- C3aR plays both sides in regulating resistance to bacterial infections.PLoS pathogens · 2022Review
- Intracellular Complement Component 3 Attenuated Ischemia-Reperfusion Injury in the Isolated Buffer-Perfused Mouse Heart and Is Associated With Improved Metabolic Homeostasis.Frontiers in immunology · 2022Article
- More than a Pore: Nonlytic Antimicrobial Functions of Complement and Bacterial Strategies for Evasion.Microbiology and molecular biology reviews : MMBR · 2021Review
- The Complement C3a and C3a Receptor Pathway in Kidney Diseases.Frontiers in immunology · 2020Review
- Circadian Clock and Complement Immune System-Complementary Control of Physiology and Pathology?Frontiers in cellular and infection microbiology · 2020Review
- Distinct roles of the anaphylatoxin receptors C3aR, C5aR1 and C5aR2 in experimental meningococcal infections.Virulence · 2019Article
- The Second Receptor for C5a, C5aR2, Is Detrimental to Mice during Systemic Infection withJournal of immunology (Baltimore, Md. : 1950) · 2019Article
- Innate and Adaptive Immune Responses duringMicrobiology spectrum · 2019Article
- Intracellular C3 Protects Human Airway Epithelial Cells from Stress-associated Cell Death.American journal of respiratory cell and molecular biology · 2019Article
- Brain microvascular endothelial cells exhibit lower activation of the alternative complement pathway than glomerular microvascular endothelial cells.The Journal of biological chemistry · 2018Article
- Gut Microbiota and Relevant Metabolites Analysis in Alcohol Dependent Mice.Frontiers in microbiology · 2018Article
- Article
- The Complement Anaphylatoxins C5a and C3a Suppress IFN-β Production in Response toJournal of immunology (Baltimore, Md. : 1950) · 2017Article
- Innate and adaptive immunologic functions of complement in the host response to Listeria monocytogenes infection.Immunobiology · 2016Review
- Whole-genome sequencing of the endangered bovine species Gayal (Bos frontalis) provides new insights into its genetic features.Scientific reports · 2016Article
- Applying complement therapeutics to rare diseases.Clinical immunology (Orlando, Fla.) · 2015Review
- Complement 5a Enhances Hepatic Metastases of Colon Cancer via Monocyte Chemoattractant Protein-1-mediated Inflammatory Cell Infiltration.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Listeria monocytogenes is a Gram-positive intracellular bacterium that is acquired through tainted food and may lead to systemic infection and possible death. Despite the importance of the innate immune system in fighting L. monocytogenes infection, little is known about the role of complement and its activation products, including the potent C3a anaphylatoxin. In a model of systemic L. monocytogenes infection, we show that mice lacking the receptor for C3a (C3aR(-/-)) are significantly more sensitive to infection compared with wild-type mice, as demonstrated by decreased survival, increased bacterial burden, and increased damage to their livers and spleens. The inability of the C3aR(-/-) mice to clear the bacterial infection was not caused by defective macrophages or by a reduction in cytokines/chemokines known to be critical in the host response to L. monocytogenes, including IFN-γ and TNF-α. Instead, TUNEL staining, together with Fas, active caspase-3, and Bcl-2 expression data, indicates that the increased susceptibility of C3aR(-/-) mice to L. monocytogenes infection was largely caused by increased L. monocytogenes-induced apoptosis of myeloid and lymphoid cells in the spleen that are required for ultimate clearance of L. monocytogenes, including neutrophils, macrophages, dendritic cells, and T cells. These findings reveal an unexpected function of C3a/C3aR signaling during the host immune response that suppresses Fas expression and caspase-3 activity while increasing Bcl-2 expression, thereby providing protection to both myeloid and lymphoid cells against L. monocytogenes-induced apoptosis.
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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.