ArticlePLoS pathogens2008
RETRACTED: The uptake of apoptotic cells drives Coxiella burnetii replication and macrophage polarization: a model for Q fever endocarditis.
Article in PLoS pathogens, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 57 citations in OpenAlex.
- TGF-β/IFN-γ Antagonism in Subversion and Self-Defense of Phase II Coxiella burnetiiInfection and immunity · 2023Trial
- Retraction: The Uptake of Apoptotic Cells Drives Coxiella burnetii Replication and Macrophage Polarization: A Model for Q Fever Endocarditis.PLoS pathogens · 2026Article
- A Comprehensive Review of the Mechanisms of Human Q Fever: Pathogenesis and Pathophysiology.Pathogens (Basel, Switzerland) · 2025Review
- Fibrous scaffolds loaded with BMSC-derived apoptotic vesicles promote wound healing by inducing macrophage polarization.Genes & diseases · 2025Article
- Susceptibility, Immunity, and Persistent Infection Drive Endemic Cycles of Coxiellosis on Dairy Farms.Animals : an open access journal from MDPI · 2024Article
- Q fever immunology: the quest for a safe and effective vaccine.NPJ vaccines · 2023Review
- Expression of Concern: The Uptake of Apoptotic Cells Drives Coxiella burnetii Replication and Macrophage Polarization: A Model for Q Fever Endocarditis.PLoS pathogens · 2022Article
- Identification and distribution of pathogens coinfecting with Brucella spp., Coxiella burnetii and Rift Valley fever virus in humans, livestock and wildlife.Zoonoses and public health · 2022Review
- To die or not to die: Programmed cell death responses and their interactions with Coxiella burnetii infection.Molecular microbiology · 2022Article
- Natural genetic variation in Drosophila melanogaster reveals genes associated with Coxiella burnetii infection.Genetics · 2021Article
- Mesenchymal Stem Cell-Macrophage Crosstalk and Maintenance of Inflammatory Microenvironment Homeostasis.Frontiers in cell and developmental biology · 2021Review
- Indoleamine 2,3-Dioxygenase Regulates Macrophage Recruitment, Polarization and Phagocytosis in Aspergillus Fumigatus Keratitis.Investigative ophthalmology & visual science · 2020Article
- Hacking the host: exploitation of macrophage polarization by intracellular bacterial pathogens.Pathogens and disease · 2020Review
- Efferocytosis and Outside-In Signaling by Cardiac Phagocytes. Links to Repair, Cellular Programming, and Intercellular Crosstalk in Heart.Frontiers in immunology · 2017Review
- Exploiting death: apoptotic immunity in microbial pathogenesis.Cell death and differentiation · 2016Review
- Apoptotic CD8 T-lymphocytes disable macrophage-mediated immunity to Trypanosoma cruzi infection.Cell death & disease · 2016Article
- Coxiella burnetii dormancy in a fatal ten-year multisystem dysfunctional illness: case report.BMC infectious diseases · 2016Article
- Microglial M1/M2 polarization and metabolic states.British journal of pharmacology · 2016Review
- Dysregulation of serum gamma interferon levels in vascular chronic Q Fever patients provides insights into disease pathogenesis.Clinical and vaccine immunology : CVI · 2015Article
- Phenotypic diversity and emerging new tools to study macrophage activation in bacterial infectious diseases.Frontiers in immunology · 2014Review
Corrections and comments
- Retraction · 2026-05-12Author Unresponsive · Concerns/Issues about Human Subject Welfare · Investigation by Company/Institution · Investigation by Journal/Publisher · Lack of IRB/IACUC Approval and/or Compliance · Upgrade/Update of Prior Notice(s) ·
- Expression of concern · 2022-12-13Investigation by Journal/Publisher · Updated to Retraction ·
- Expression of concern
- Retracted
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patients with valvulopathy have the highest risk to develop infective endocarditis (IE), although the relationship between valvulopathy and IE is not clearly understood. Q fever endocarditis, an IE due to Coxiella burnetii, is accompanied by immune impairment. Patients with valvulopathy exhibited increased levels of circulating apoptotic leukocytes, as determined by the measurement of active caspases and nucleosome determination. The binding of apoptotic cells to monocytes and macrophages, the hosts of C. burnetii, may be responsible for the immune impairment observed in Q fever endocarditis. Apoptotic lymphocytes (AL) increased C. burnetii replication in monocytes and monocyte-derived macrophages in a cell-contact dependent manner, as determined by quantitative PCR and immunofluorescence. AL binding induced a M2 program in monocytes and macrophages stimulated with C. burnetii as determined by a cDNA chip containing 440 arrayed sequences and functional tests, but this program was in part different in monocytes and macrophages. While monocytes that had bound AL released high levels of IL-10 and IL-6, low levels of TNF and increased CD14 expression, macrophages that had bound AL released high levels of TGF-beta1 and expressed mannose receptor. The neutralization of IL-10 and TGF-beta1 prevented the replication of C. burnetii due to the binding of AL, suggesting that they were critically involved in bacterial replication. In contrast, the binding of necrotic cells to monocytes and macrophages led to C. burnetii killing and typical M1 polarization. Finally, interferon-gamma corrected the immune deactivation induced by apoptotic cells: it prevented the replication of C. burnetii and re-directed monocytes and macrophages toward a M1 program, which was deleterious for C. burnetii. We suggest that leukocyte apoptosis associated with valvulopathy may be critical for the pathogenesis of Q fever endocarditis by deactivating immune cells and creating a favorable environment for bacterial persistence.
Indexed as
Identifiers
What OpenQuestion holds
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.