ArticlePLoS pathogens2015
Brucella abortus Induces the Premature Death of Human Neutrophils through the Action of Its Lipopolysaccharide.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 51 citations in OpenAlex.
- Complementary Use of Probiotics and Their Antimicrobial Proteins in Brucellosis: A Comprehensive Review of Mechanisms and Clinical Benefits.Probiotics and antimicrobial proteins · 2026Review
- Enhanced immunogenicity of theFrontiers in immunology · 2026Article
- Brucella abortus impairs T lymphocyte responsiveness by mobilizing IL-1RA-secreting omental neutrophils.Nature communications · 2025Article
- Assessment of immune responses toFrontiers in immunology · 2025Article
- Brucellosis: Bacteriology, pathogenesis, epidemiology and role of the metallophores in virulence: a review.Frontiers in cellular and infection microbiology · 2025Review
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- Cell and Tissue Tropism of Brucella spp.Infection and immunity · 2023Review
- Expression of NLRP3 and AIM2 inflammasome in Peripheral blood in Chinese patients with acute and chronic brucellosis.Scientific reports · 2022Article
- Immunosuppressive Mechanisms in Brucellosis in Light of Chronic Bacterial Diseases.Microorganisms · 2022Review
- A gene expression map of host immune response in human brucellosis.Frontiers in immunology · 2022Article
- The Mechanism of Facultative Intracellular Parasitism ofInternational journal of molecular sciences · 2021Review
- Uncovering the Hidden Credentials ofMicrobiology and molecular biology reviews : MMBR · 2021Review
- Review
- Small ubiquitin-related modifier 2 affects the intracellular survival ofInnate immunity · 2021Article
- The Role of Neutrophils in Brucellosis.Microbiology and molecular biology reviews : MMBR · 2020Review
- The Twin-Arginine Translocation System Is Important for Stress Resistance and Virulence of Brucella melitensis.Infection and immunity · 2020Article
- Modulatory Effect of Linoleic Acid DuringJournal of microbiology and biotechnology · 2020Article
- β-Sitosterol Contributes in the Resistance to Invasion and Survival ofJournal of microbiology and biotechnology · 2020Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Most bacterial infections induce the activation of polymorphonuclear neutrophils (PMNs), enhance their microbicidal function, and promote the survival of these leukocytes for protracted periods of time. Brucella abortus is a stealthy pathogen that evades innate immunity, barely activates PMNs, and resists the killing mechanisms of these phagocytes. Intriguing clinical signs observed during brucellosis are the low numbers of Brucella infected PMNs in the target organs and neutropenia in a proportion of the patients; features that deserve further attention. Here we demonstrate that B. abortus prematurely kills human PMNs in a dose-dependent and cell-specific manner. Death of PMNs is concomitant with the intracellular Brucella lipopolysaccharide (Br-LPS) release within vacuoles. This molecule and its lipid A reproduce the premature cell death of PMNs, a phenomenon associated to the low production of proinflammatory cytokines. Blocking of CD14 but not TLR4 prevents the Br-LPS-induced cell death. The PMNs cell death departs from necrosis, NETosis and classical apoptosis. The mechanism of PMN cell death is linked to the activation of NADPH-oxidase and a modest but steadily increase of ROS mediators. These effectors generate DNA damage, recruitments of check point kinase 1, caspases 5 and to minor extent of caspase 4, RIP1 and Ca++ release. The production of IL-1β by PMNs was barely stimulated by B. abortus infection or Br-LPS treatment. Likewise, inhibition of caspase 1 did not hamper the Br-LPS induced PMN cell death, suggesting that the inflammasome pathway was not involved. Although activation of caspases 8 and 9 was observed, they did not seem to participate in the initial triggering mechanisms, since inhibition of these caspases scarcely blocked PMN cell death. These findings suggest a mechanism for neutropenia in chronic brucellosis and reveal a novel Brucella-host cross-talk through which B. abortus is able to hinder the innate function of PMN.
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