ArticleInfection and immunity2008
CCL28 is increased in human Helicobacter pylori-induced gastritis and mediates recruitment of gastric immunoglobulin A-secreting cells.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- Role of mucosal chemokines in the development of tissue-resident CD4Frontiers in immunology · 2026Review
- Precancerous pathways to gastric cancer: a review of experimental animal models recapitulating the correa cascade.Frontiers in cell and developmental biology · 2025Review
- Article
- Current study of pathogenetic mechanisms and therapeutics of chronic atrophic gastritis: a comprehensive review.Frontiers in cell and developmental biology · 2024Review
- Expression of Chemokine CCL28 in Ulcerative Colitis Patients.Gut and liver · 2021Article
- The CCL28 levels are elevated in the serum of patients with irritable bowel syndrome and associated with the clinical symptoms.American journal of clinical and experimental immunology · 2021Article
- Deficiency of Stomach-Type Claudin-18 in Mice Induces Gastric Tumor Formation Independent of H pylori Infection.Cellular and molecular gastroenterology and hepatology · 2019Article
- Regulatory T cells control endothelial chemokine production and migration of T cells into intestinal tumors of APCCancer immunology, immunotherapy : CII · 2018Article
- CCL28 chemokine: An anchoring point bridging innate and adaptive immunity.International immunopharmacology · 2017Review
- The role of C1q in recognition of apoptotic epithelial cells and inflammatory cytokine production by phagocytes during Helicobacter pylori infection.Journal of inflammation (London, England) · 2015Article
- Impaired migration of IgA-secreting cells to colon adenocarcinomas.Cancer immunology, immunotherapy : CII · 2013Article
- Enhanced expression of CXCL13 in human Helicobacter pylori-associated gastritis.Digestive diseases and sciences · 2011Article
- Sublingual immunization protects against Helicobacter pylori infection and induces T and B cell responses in the stomach.Infection and immunity · 2010Article
- The antimicrobial activity of CCL28 is dependent on C-terminal positively-charged amino acids.European journal of immunology · 2010Article
- Regulation of gastric B cell recruitment is dependent on IL-17 receptor A signaling in a model of chronic bacterial infection.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Selective upregulation of endothelial E-selectin in response to Helicobacter pylori-induced gastritis.Infection and immunity · 2009Article
- Enhanced expression of CCL20 in human Helicobacter pylori-associated gastritis.Clinical immunology (Orlando, Fla.) · 2009Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human Helicobacter pylori infection gives rise to an active chronic gastritis and is a major risk factor for the development of duodenal ulcer disease and gastric adenocarcinoma. The infection is accompanied by a large accumulation of immunoglobulin A (IgA)-secreting cells in the gastric mucosa, and following mucosal immunization only H. pylori-infected volunteers mounted a B-cell response in the gastric mucosa. To identify the signals for recruitment of gastric IgA-secreting cells, we investigated the gastric production of CCL28 (mucosa-associated epithelial chemokine) and CCL25 (thymus-expressed chemokine) in H. pylori-infected and uninfected individuals and the potential of gastric B-cell populations to migrate toward these chemokines. Gastric tissue from H. pylori-infected individuals contained significantly more CCL28 protein and mRNA than that from uninfected individuals, while CCL25 levels remained unchanged. Chemokine-induced migration of gastric lamina propria lymphocytes isolated from patients undergoing gastric resection was then assessed using the Transwell system. IgA-secreting cells and IgA(+) memory B cells from H. pylori-infected tissues migrated toward CCL28 but not CCL25, while the corresponding cells from uninfected patients did not. Furthermore, IgG-secreting cells from H. pylori-infected patients did not migrate to CCL28 but instead to CXCL12 (SDF-1alpha). However, chemokine receptor expression did not correlate to the migratory pattern of the different B-cell populations. These studies are the first to show increased CCL28 production during gastrointestinal infection in humans and provide an explanation for the large influx of IgA-secreting cells to the gastric mucosa in H. pylori-infected individuals.
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