ArticlePloS one2009
Inefficient Toll-like receptor-4 stimulation enables Bordetella parapertussis to avoid host immunity.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Modeling the catarrhal stage of Bordetella pertussis upper respiratory tract infections in mice.Disease models & mechanisms · 2022Article
- Enhancement of immune response against Bordetella spp. by disrupting immunomodulation.Scientific reports · 2019Article
- Article
- Immunomodulation as a Novel Strategy for Prevention and Treatment ofFrontiers in immunology · 2019Review
- Bordetella parapertussis Circumvents Neutrophil Extracellular Bactericidal Mechanisms.PloS one · 2017Article
- Bordetella parapertussis PagP mediates the addition of two palmitates to the lipopolysaccharide lipid A.Journal of bacteriology · 2015Article
- The regulatory toll-like receptor 4 genetic polymorphism rs11536889 is associated with renal, coagulation and hepatic organ failure in sepsis patients.Journal of translational medicine · 2014Article
- Article
- Lipopolysaccharide clearance, bacterial clearance, and systemic inflammatory responses are regulated by cell type-specific functions of TLR4 during sepsis.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Article
- Contribution of Bordetella filamentous hemagglutinin and adenylate cyclase toxin to suppression and evasion of interleukin-17-mediated inflammation.Infection and immunity · 2012Article
- Prevalence and clinical course in invasive infections with meningococcal endotoxin variants.PloS one · 2012Article
- Enhancement of Bordetella parapertussis infection by Bordetella pertussis in mixed infection of the respiratory tract.FEMS immunology and medical microbiology · 2011Article
- Phosphoryl moieties of lipid A from Neisseria meningitidis and N. gonorrhoeae lipooligosaccharides play an important role in activation of both MyD88- and TRIF-dependent TLR4-MD-2 signaling pathways.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Acellular pertussis vaccination facilitates Bordetella parapertussis infection in a rodent model of bordetellosis.Proceedings. Biological sciences · 2010Article
- The structure of Neisseria meningitidis lipid A determines outcome in experimental meningococcal disease.Infection and immunity · 2010Article
- Tobacco upregulates P. gingivalis fimbrial proteins which induce TLR2 hyposensitivity.PloS one · 2010Article
- IL-10 induction by Bordetella parapertussis limits a protective IFN-gamma response.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- The O antigen is a critical antigen for the development of a protective immune response to Bordetella parapertussis.Infection and immunity · 2009Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The recognition of bacterial lipopolysaccharide (LPS) by host Toll-like receptor (TLR)4 is a crucial step in developing protective immunity against several gram negative bacterial pathogens. Bordetella bronchiseptica and B. pertussis stimulate robust TLR4 responses that are required to control the infection, but a close relative, B. parapertussis, poorly stimulates this receptor, and TLR4 deficiency does not affect its course of infection. This led us to hypothesize that inefficient TLR4 stimulation enables B. parapertussis to evade host immunity. In a mouse model of infection, B. parapertussis grew rapidly in the lungs, but no measurable increase in TLR4-mediated cytokine, chemokine, or leukocyte responses were observed over the first few days of infection. Delivery of a TLR4 stimulant in the inoculum resulted in a robust inflammatory response and a 10- to 100-fold reduction of B. parapertussis numbers. As we have previously shown, B. parapertussis grows efficiently during the first week of infection even in animals passively immunized with antibodies. We show that this evasion of antibody-mediated clearance is dependent on the lack of TLR4 stimulation by B. parapertussis as co-inoculation with a TLR4 agonist resulted in 10,000-fold lower B. parapertussis numbers on day 3 in antibody-treated wild type, but not TLR4-deficient, mice. Together, these results indicate that inefficient TLR4 stimulation by B. parapertussis enables it to avoid host immunity and grow to high numbers in the respiratory tract of naïve and immunized hosts.
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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.