ArticleCell communication and signaling : CCS2013
The Campylobacter jejuni CiaD effector protein activates MAP kinase signaling pathways and is required for the development of disease.
Article in Cell communication and signaling : CCS, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 62 citations in OpenAlex.
- Infections and Syndromes Caused by Campylobacter.Microorganisms · 2026Review
- Cytoplasmic and nuclear extracellular signal-regulated kinases are necessary forFrontiers in microbiology · 2026Article
- Campylobacter jejuni regulates cell cycle progression to potentiate host cell invasion.Cell communication and signaling : CCS · 2025Article
- Review
- Pathogenicity and virulence ofVirulence · 2024Review
- Campylobacter jejuni virulence factors: update on emerging issues and trends.Journal of biomedical science · 2024Review
- Gut metabolite L-lactate supportsProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Campylobacter jejuni: targeting host cells, adhesion, invasion, and survival.Applied microbiology and biotechnology · 2023Review
- The Missing Pieces: The Role of Secretion Systems inBiomolecules · 2023Review
- Zoonotic Transmission ofFrontiers in microbiology · 2022Article
- Campylobacter jejuni Triggers Signaling through Host Cell Focal Adhesions To Inhibit Cell Motility.mBio · 2021Article
- Campylobacter jejuni genotypes are associated with post-infection irritable bowel syndrome in humans.Communications biology · 2021Article
- The Host Cellular Immune Response to Infection by Campylobacter Spp. and Its Role in Disease.Infection and immunity · 2021Review
- Bacterial Flagellar Filament: A Supramolecular Multifunctional Nanostructure.International journal of molecular sciences · 2021Review
- The Campylobacter jejuni CiaD effector co-opts the host cell protein IQGAP1 to promote cell entry.Nature communications · 2021Article
- Metal homeostasis in pathogenic Epsilonproteobacteria: mechanisms of acquisition, efflux, and regulation.Metallomics : integrated biometal science · 2021Review
- Multi-Omics Approach Reveals the Potential Core Vaccine Targets for the Emerging Foodborne PathogenFrontiers in microbiology · 2021Article
- Microbiota attenuates chicken transmission-exacerbated campylobacteriosis in Il10Scientific reports · 2020Article
- Peptidase PepP is a novel virulence factor ofGut microbes · 2020Article
- A porcine ligated loop model reveals new insight into the host immune response againstGut microbes · 2020Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundEnteric pathogens utilize a distinct set of proteins to modulate host cell signaling events that promote host cell invasion, induction of the inflammatory response, and intracellular survival. Human infection with Campylobacter jejuni, the causative agent of campylobacteriosis, is characterized by diarrhea containing blood and leukocytes. The clinical presentation of acute disease, which is consistent with cellular invasion, requires the delivery of the Campylobacter invasion antigens (Cia) to the cytosol of host cells via a flagellar Type III Secretion System (T3SS). We identified a novel T3SS effector protein, which we termed CiaD that is exported from the C. jejuni flagellum and delivered to the cytosol of host cells.
resultsWe show that the host cell kinases p38 and Erk 1/2 are activated by CiaD, resulting in the secretion of interleukin-8 (IL-8) from host cells. Additional experiments revealed that CiaD-mediated activation of p38 and Erk 1/2 are required for maximal invasion of host cells by C. jejuni. CiaD contributes to disease, as evidenced by infection of IL-10 knockout mice. Noteworthy is that CiaD contains a Mitogen-activated protein (MAP) kinase-docking site that is found within effector proteins produced by other enteric pathogens. These findings indicate that C. jejuni activates the MAP kinase signaling pathways Erk 1/2 and p38 to promote cellular invasion and the release of the IL-8 pro-inflammatory chemokine.
conclusionsThe identification of a novel T3SS effector protein from C. jejuni significantly expands the knowledge of virulence proteins associated with C. jejuni pathogenesis and provides greater insight into the mechanism utilized by C. jejuni to invade host cells.
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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.