Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Impact of cagPAI and T4SS on the inflammatory response of human neutrophils to Helicobacter pylori infection.

PloS one - 1 Jan 2014

Sánchez-Zauco Norma Angélica, Torres Javier, Pérez-Figueroa Gloria Erandi, Álvarez-Arellano Lourdes, Camorlinga-Ponce Margarita, Gómez Alejandro, Giono-Cerezo Silvia, Maldonado-Bernal Carmen

Abstract excerpt

Helicobacter pylori contains a pathogenicity island, cagPAI, with genes homologous to components of the type IV secretion system (T4SS) of Agrobacterium tumefaciens. The T4SS components assemble a structure that transfers CagA protein and peptidoglycan into host epithelial cells, causing the increased release of interleukin 8 (IL8) from the cells. The Toll-like receptors on neutrophils recognize H. pylori,...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Bacterial Secretion Systems
Share to Down-Regulation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Genomic Islands

Share to Helicobacter Infections

Share to Helicobacter pylori

Share to Inflammation

Share to Neutrophils

Share to Toll-Like Receptors

Source

Open in PubMed Open full text

Identifiers

PMID: 23755130
DOI: 10.1371/journal.pone.0064623
PMCID: PMC3670914

Genes

TLR9

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Impact of cagPAI and T4SS on the inflammatory response of human neutrophils to Helicobacter pylori infection.PMID 23755130Read ↗

Activation of NLRP3 inflammasome in human neutrophils by Helicobacter pylori infectionSemantic proximity Read ↗

Unveiling the crucial role of type IV secretion system and motility of <i>Helicobacter pylori</i> in IL-1β production via NLRP3 inflammasome activation in neutrophilsSemantic proximity Read ↗

Macrophages recognize the Helicobacter pylori type IV secretion system in the absence of toll-like receptor signallingSemantic proximity Read ↗

Differential inflammatory response to Helicobacter pylori infection: etiology and clinical outcomesSemantic proximity Read ↗

TIFA Signaling in Gastric Epithelial Cells Initiates the cag Type 4 Secretion System-Dependent Innate Immune Response to Helicobacter pylori InfectionSemantic proximity Read ↗

Interplay of the Gastric Pathogen<i>Helicobacter pylori</i>with Toll-Like ReceptorsSemantic proximity Read ↗

<i>Helicobacter pylori</i>neutrophil-activating protein: From molecular pathogenesis to clinical applicationsSemantic proximity Read ↗

Toll-like Receptor 5 Activation by the CagY Repeat Domains of Helicobacter pyloriSemantic proximity Read ↗

A novel NOD1- and CagA-independent pathway of interleukin-8 induction mediated by the Helicobacter pylori type IV secretion system.Semantic proximity Read ↗

Helicobacter pylori Pathogen-Associated Molecular Patterns: Friends or Foes?Semantic proximity Read ↗

The neutrophil-activating protein of Helicobacter pylori promotes Th1 immune responses.Semantic proximity Read ↗

Helicobacter pylori CagA and Cag type IV secretion system activity have key roles in triggering gastric transcriptional and proteomic alterationsSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.