ArticleInfection and immunity2010
Substitution of the Bordetella pertussis lipid A phosphate groups with glucosamine is required for robust NF-kappaB activation and release of proinflammatory cytokines in cells expressing human but not murine Toll-like receptor 4-MD-2-CD14.
Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Cross talk between bacterial and human gene networks enriched using ncRNAs in IBD disease.Scientific reports · 2023Pooled it
- Review
- Mechanisms of Pertussis Toxin Action: ADP-Ribosylation and Its Role in Pertussis Pathogenesis.Toxins · 2026Review
- CD4+ T-cell immunity toDiscover immunity · 2026Review
- Article
- Determining theFrontiers in microbiology · 2025Article
- A whole-cell pertussis vaccine engineered to elicit reduced reactogenicity protects baboons against pertussis challenge.mSphere · 2024Article
- Programming Bordetella pertussis lipid A to promote adjuvanticity.Microbial cell factories · 2024Article
- Diversity, Complexity, and Specificity of Bacterial Lipopolysaccharide (LPS) Structures Impacting Their Detection and Quantification.International journal of molecular sciences · 2024Article
- Modeling the catarrhal stage of Bordetella pertussis upper respiratory tract infections in mice.Disease models & mechanisms · 2022Article
- Lipid A heterogeneity and its role in the host interactions with pathogenic and commensal bacteria.microLife · 2022Review
- Reduction of endotoxicity in Bordetella bronchiseptica by lipid A engineering: Characterization of lpxL1 and pagP mutants.Virulence · 2021Article
- Pathogenicity and virulence ofVirulence · 2021Review
- Bordetella bronchiseptica Glycosyltransferase Core Mutants Trigger Changes in Lipid A Structure.Journal of the American Society for Mass Spectrometry · 2019Article
- Bordetella holmesii: Lipid A Structures and Corresponding Genomic Sequences Comparison in Three Clinical Isolates and the Reference Strain ATCC 51541.International journal of molecular sciences · 2017Article
- Antimicrobial Peptide Resistance Genes in the Plant Pathogen Dickeya dadantii.Applied and environmental microbiology · 2016Article
- Article
- Review of the neutrophil response to Bordetella pertussis infection.Pathogens and disease · 2015Review
- Bordetella pertussis Lipid A Recognition by Toll-like Receptor 4 and MD-2 Is Dependent on Distinct Charged and Uncharged Interfaces.The Journal of biological chemistry · 2015Article
- Bordetella pertussis lipid A glucosamine modification confers resistance to cationic antimicrobial peptides and increases resistance to outer membrane perturbation.Antimicrobial agents and chemotherapy · 2014Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bordetella pertussis endotoxin is a key modulator of the host immune response, mainly due to the role of its lipid A moiety in Toll-like receptor 4 (TLR4)-mediated signaling. We have previously demonstrated that the lipid A phosphate groups of B. pertussis BP338 can be substituted with glucosamine in a BvgAS-regulated manner. Here we examined the effect of this lipid A modification on the biological activity of B. pertussis endotoxin. We compared purified endotoxin and heat-killed B. pertussis BP338 whole cells that have modified lipid A phosphate groups to an isogenic mutant lacking this modification with respect to their capacities to induce the release of inflammatory cytokines by human and murine macrophages and to participate in the TLR4-mediated activation of NF-kappaB in transfected HEK-293 cells. We found inactivated B. pertussis cells to be stronger inducers of proinflammatory cytokines in THP-1-derived macrophages when lipid A was modified. Most notably, lack of lipid A modification abolished the ability of purified B. pertussis endotoxin to induce the release of inflammatory cytokines by human THP-1-derived macrophages but led to only slightly reduced inflammatory cytokine levels when stimulating murine (RAW 264.7) macrophages. Accordingly, upon stimulation of HEK-293 cells with inactivated bacteria and purified endotoxin, lack of lipid A modification led to impaired NF-kappaB activation only when human, and not when murine, TLR4-MD-2-CD14 was expressed. We speculate that in B. pertussis, lipid A modification has evolved to benefit the bacteria during human infection by modulating immune defenses rather than to evade innate immune recognition.
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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.