ArticleJournal of clinical pathology2007
Involvement of mast cells in gastritis caused by Helicobacter pylori: a potential role in epithelial cell apoptosis.
Article in Journal of clinical pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- The Potential Role ofMicroorganisms · 2025Review
- Impact of Mast Cell Activation on Neurodegeneration: A Potential Role for Gut-Brain Axis andNeurology international · 2024Review
- The Role ofJournal of clinical medicine · 2024Review
- Impact ofFrontiers in gastroenterology (Lausanne, Switzerland) · 2024Review
- Article
- Helicobacter pylori-induced IL-33 modulates mast cell responses, benefits bacterial growth, and contributes to gastritis.Cell death & disease · 2018Article
- Morphological and Cellular Features of Innate Immune Reaction in Helicobacter pylori Gastritis: A Brief Review.International journal of molecular sciences · 2016Review
- Article
- Eosinophils and mast cells as therapeutic targets in pediatric functional dyspepsia.World journal of gastrointestinal pharmacology and therapeutics · 2013Review
- Plasticity in mast cell responses during bacterial infections.Current opinion in microbiology · 2012Review
- FcepsilonRI-mediated mast cell migration: signaling pathways and dependence on cytosolic free Ca2+ concentration.Cellular signalling · 2009Article
- LANA-1, Bcl-2, Mcl-1 and HIF-1alpha protein expression in HIV-associated Kaposi sarcoma.Virchows Archiv : an international journal of pathology · 2009Article
- Review
- Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe role(s) of mast cells (MC) in gastric mucosal inflammation caused by Helicobacterpylori is (are) still debated.
aimTo determine whether there is an association between MC density and epithelial cell apoptosis in antral gastric mucosa infected by H pylori. PATIENTS AND
methodsBiopsy specimens from 122 H pylori-positive subjects with chronic active gastritis, 84 patients with non-steroidal anti-inflammatory drug-induced gastritis and 48 volunteers were included. H pylori genotypes were determined by PCR amplification of bacterial cultures. Immunohistochemical analysis was performed on tissue microarrays with anti-CD117, anti-chymase, anti-tryptase, anti-myeloperoxidase, anti-Bcl-2, anti-Bcl-x, anti-Bax and anti-caspase 3 antibodies.
resultsOf the 122 patients infected with H pylori, 76 (62.3%) harboured cagA positive strains. H pylori isolates belonged to the vacAs1/m1 genotype in 82 (67%) cases, to the vacAs2/m2 genotype in 23 (18.8%) cases and to the vacAs1/m2 genotype in 17 (13.9%) cases. 61 (50%) H pylori isolates were babA2+. In patients infected with H pylori, the density of MC, and in particular the number of MC-associated epithelial cells, was correlated with a high number of apoptotic epithelial cells. Moreover, the density of MC was correlated with the number of neutrophils infiltrating the antral gastric mucosa, and was strongly increased in patients infected with cagA, vacAs1/m1 and babA2 positive strains.
conclusionsTaken together, these data show that the density of MC can be considered as a histopathological criterion of gastritis activity in patients infected with H pylori.
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Registered trials
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