ArticleJournal of leukocyte biology2011
Neisseria meningitidis capsular polysaccharides induce inflammatory responses via TLR2 and TLR4-MD-2.
Article in Journal of leukocyte biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 64 citations in OpenAlex.
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- The Changes in Bacterial Microbiome Associated with Immune Disorder in Allergic Respiratory Disease.Microorganisms · 2022Review
- Neuronal Damage and Neuroinflammation, a Bridge Between Bacterial Meningitis and Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2021Article
- Interactions and Signal Transduction Pathways Involved during Central Nervous System Entry byInternational journal of molecular sciences · 2020Review
- Comparative Study of Immunogenic Properties of Purified Capsular Polysaccharides fromInfection and immunity · 2020Article
- Better Adjuvants for Better Vaccines: Progress in Adjuvant Delivery Systems, Modifications, and Adjuvant-Antigen Codelivery.Vaccines · 2020Review
- Identification of aPathogens (Basel, Switzerland) · 2020Article
- Sugar-Coated Killer: Serotype 3 Pneumococcal Disease.Frontiers in cellular and infection microbiology · 2020Review
- Weak Agonistic LPS Restores Intestinal Immune Homeostasis.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
- Article
- Analysis of novel meningococcal vaccine formulations.Human vaccines & immunotherapeutics · 2017Article
- Entirely Carbohydrate-Based Vaccines: An Emerging Field for Specific and Selective Immune Responses.Vaccines · 2016Review
- A Choroid Plexus Epithelial Cell-based Model of the Human Blood-Cerebrospinal Fluid Barrier to Study Bacterial Infection from the Basolateral Side.Journal of visualized experiments : JoVE · 2016Article
- Article
- The role of Toll-like receptor 4 polymorphisms in vaccine immune response.The pharmacogenomics journal · 2016Review
- Free exopolysaccharide from Mycoplasma mycoides subsp. mycoides possesses anti-inflammatory properties.Veterinary research · 2015Article
- Effect of TNF-α inhibitors on transcriptional levels of pro-inflammatory interleukin-33 and Toll-like receptors-2 and -9 in psoriatic plaques.Experimental and therapeutic medicine · 2015Article
- How the Knowledge of Interactions between Meningococcus and the Human Immune System Has Been Used to Prepare Effective Neisseria meningitidis Vaccines.Journal of immunology research · 2015Review
- Phosphoethanolamine Modification of Neisseria gonorrhoeae Lipid A Reduces Autophagy Flux in Macrophages.PloS one · 2015Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
CPS are major virulence factors in infections caused by Neisseria meningitidis and form the basis for meningococcal serogroup designation and protective meningococcal vaccines. CPS polymers are anchored in the meningococcal outer membrane through a 1,2-diacylglycerol moiety, but the innate immunostimulatory activity of CPS is largely unexplored. Well-established human and murine macrophage cell lines and HEK/TLR stably transfected cells were stimulated with CPS, purified from an endotoxin-deficient meningococcal serogroup B NMB-lpxA mutant. CPS induced inflammatory responses via TLR2- and TLR4-MD-2. Meningococcal CPS induced a dose-dependent release of cytokines (TNF-α, IL-6, IL-8, and CXCL10) and NO from human and murine macrophages, respectively. CPS induced IL-8 release from HEK cells stably transfected with TLR2/6, TLR2, TLR2/CD14, and TLR4/MD-2/CD14 but not HEK cells alone. mAb to TLR2 but not an isotype control antibody blocked CPS-induced IL-8 release from HEK-TLR2/6-transfected cells. A significant reduction in TNF-α and IL-8 release was seen when THP-1- and HEK-TLR4/MD-2-CD14- but not HEK-TLR2- or HEK-TLR2/6-transfected cells were stimulated with CPS in the presence of Eritoran (E5564), a lipid A antagonist that binds to MD-2, and a similar reduction in NO and TNF-α release was also seen in RAW 264.7 cells in the presence of Eritoran. CD14 and LBP enhanced CPS bioactivity, and NF-κB was, as anticipated, the major signaling pathway. Thus, these data suggest that innate immune recognition of meningococcal CPS by macrophages can occur via TLR2- and TLR4-MD-2 pathways.
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Registered trials
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