Eosinophils and mast cells in chronic gastritis: possible implications in carcinogenesis

Abstract

Eosinophils and mast cells participate in the immune response against Helicobacter pylori, but their involvement in the gastric precancerous process is unclear. This study aimed to estimate eosinophil and mast cell density in antral mucosa in subjects from two Colombian populations with contrasting gastric cancer risks. Gastric mucosa biopsies were collected from 117 adult males (72 from a highrisk area and 45 from a low-risk area). A histopathology score was used to quantify severity of the lesions. Quantitation of eosinophils in hematoxylin-eosin stained sections and mast cells in immunostained sections for CD117/c-Kit was performed. Helicobacter pylori infection and genotyping were assessed in Steiner stain and PCR, respectively. Logistic regression models and semi-parametric cubic smoothing splines were used for analysis of the results. Eosinophil density was significantly higher in subjects from the low-risk area compared with subjects from the highrisk area. In both populations, eosinophil density increased with the histopathology score in the progression of lesions from normal morphology to multifocal atrophic gastritis. Intestinal metaplasia and dysplasia specimens showed further increase in eosinophil density in the high-risk area, but an abrupt decrease in the low-risk area. Mast cell density increased in parallel to the histopathology score in both populations. Our results suggest that eosinophils play a dual role in chronic gastritis. In the low-risk area, elevated eosinophil density represents a Th2-biased response that may downregulate the effects of proinflammatory cytokines preventing cancer development. In contrast, in the high-risk area, eosinophils might promote a Th1-type response leading to progression of precancerous lesions.

Mast cells and eosinophils: the two key effector cells in allergic inflammation

“…Interestingly, two recent studies by Caruso et al [78] and by Piazuelo et al [79] demonstrated the formation of mast cell-eosinophil couples in gastric carcinomas and chronic gastritis, respectively, showing a clear cut interface. In addition, the cross-talk between mast cells and eosinophils was also proven in Crohn's disease and Ascaris infection [80].…”

Phylogeographic origin of Helicobacter pylori is a determinant of gastric cancer risk

“…People living in the mountains are mostly ‘Mestizos’ of Amerindian descent with European admixture, dating from the Spanish colonisation period, whereas people living in the coastal region are predominantly ‘Mulattos’ of mixed African and European ancestry 18. Although strain-specific variations in H pylori genetic content have been implicated in gastric carcinogenesis,7–9 the prevalence of cagA + vacA s1m1 H pylori strains in the LR region of Colombia is only slightly (13%) lower than in the HR region,17 and this difference in strain characteristics is not sufficient to account for a 25-fold difference in cancer rate.…”

Dual effects of Helicobacter pylori vacuolating cytotoxin on human eosinophil apoptosis in early and late periods of stimulation

“…Eosinophil degranulation in mucosal tissues plays pathogenic roles in several diseases [5][6][7]. Considering that H. pylori-induced chronic gastritis results in increased infiltration of eosinophils and that infiltrated eosinophils may mediate pathogenic effects in H. pylori-infected chronic gastric patients [8], it is possible that the infiltrated eosinophils cause tissue damage. However, the status of eosinophils induced by H. pylori infection remains unclear.…”