ArticleInfection and immunity2009
Campylobacter jejuni-induced activation of dendritic cells involves cooperative signaling through Toll-like receptor 4 (TLR4)-MyD88 and TLR4-TRIF axes.
Article in Infection and immunity, 2009. 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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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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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.
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Who cites it
36 citing papers in PubMed, 62 citations in OpenAlex.
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- The Host Cellular Immune Response to Infection by Campylobacter Spp. and Its Role in Disease.Infection and immunity · 2021Review
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- Murine Models for the Investigation of Colonization Resistance and Innate Immune Responses in Campylobacter Jejuni Infections.Current topics in microbiology and immunology · 2021Article
- Campylobacter Virulence Factors and Molecular Host-Pathogen Interactions.Current topics in microbiology and immunology · 2021Review
- Toll-Like Receptor-4 Is Involved in Mediating Intestinal and Extra-Intestinal Inflammation inMicroorganisms · 2020Article
- Induction of neutrophil extracellular traps by Campylobacter jejuni.Cellular microbiology · 2020Article
- Toll-Like Receptor-4 Dependent Intestinal and Systemic Sequelae Following PeroralPathogens (Basel, Switzerland) · 2020Article
- Novel ClinicalMicroorganisms · 2020Review
- C-Type Lectin Receptors in Host Defense Against Bacterial Pathogens.Frontiers in cellular and infection microbiology · 2020Review
- Human Immunity AgainstImmune network · 2019Review
- NovelJournal of lipid research · 2018Article
- Guillain-Barré syndrome, transverse myelitis and infectious diseases.Cellular & molecular immunology · 2018Review
- Host-specific differences in the response of cultured macrophages to Campylobacter jejuni capsule and O-methyl phosphoramidate mutants.Veterinary research · 2018Article
- Hypoacylated LPS from Foodborne PathogenFrontiers in cellular and infection microbiology · 2018Article
- Campylobacter jejuni and associated immune mechanisms: short-term effects and long-term implications for infants in low-income countries.Current opinion in infectious diseases · 2017Review
- TLR4 and TLR21 expression, MIF, IFN-β, MD-2, CD14 activation, and sIgA production in chickens administered with EFAL41 strain challenged with Campylobacter jejuni.Folia microbiologica · 2017Article
- Transcriptomic and proteomic analyses reveal key innate immune signatures in the host response to the gastrointestinal pathogen Campylobacter concisus.Infection and immunity · 2015Article
- Pseudaminic acid on Campylobacter jejuni flagella modulates dendritic cell IL-10 expression via Siglec-10 receptor: a novel flagellin-host interaction.The Journal of infectious diseases · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Campylobacter jejuni is an important cause of human enteritis and has been linked to the development of autoimmune diseases. Recently we showed that infection of murine dendritic cells (DCs) with C. jejuni resulted in DC activation and induction of Campylobacter-specific Th1-effector responses. Toll-like receptor (TLR) signaling through myeloid differentiation factor 88 (MyD88) and/or Toll-interleukin 1 (IL-1) receptor domain-containing adaptor-inducing beta interferon (IFN-beta) (TRIF) is critical in inducing immunity against pathogens. In this study, we investigated the role of TLR2, TLR4, MyD88, and TRIF signaling in C. jejuni-induced inflammatory activation of DCs. DC upregulation of major histocompatibility complex class II and costimulatory molecules after C. jejuni challenge was profoundly impaired by TLR2, TLR4, MyD88, and TRIF deficiencies. Similarly, C. jejuni-induced secretion of IL-12, IL-6, and tumor necrosis factor alpha was significantly inhibited in TLR2(-/-), TLR4(-/-), MyD88(-/-), and TRIF(-/-) DCs compared to that in wild-type DCs; however, the magnitude of inhibition was greater in MyD88(-/-), TRIF(-/-), and TLR4(-/-) DCs than in TLR2(-/-) DCs. Furthermore, C. jejuni induced interferon regulatory factor 3 phosphorylation and IFN-beta secretion by DCs in a TLR4-TRIF-dependent fashion, further demonstrating activation of this pathway by C. jejuni. Importantly, TLR2, TLR4, MyD88, and TRIF deficiencies all markedly impaired the Th1-priming ability of C. jejuni-infected DCs. Thus, our results show that cooperative signaling through the TLR4-MyD88 and TLR4-TRIF axes represents a novel mechanism mediating C. jejuni-induced inflammatory responses of DCs. To our knowledge, such a mechanism has not been demonstrated previously for an intact bacterium.
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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.