Abstract
Aim. The role of mast cells in cell-cell immune interactions has received increasing attention, although their functional interaction with neutrophils still remains to be clarified in tumors. The aim of the present study was to investigate the association between mast cells and neutrophils in a series of gastric carcinomas (GC). Patients and Methods. 52 surgically resected GC specimens were routinely processed for both light and electron microscopy. Only cases showing both mast cells and neutrophils in the tumor stroma were considered in the analysis. Results. Only 9 GC (M : F = 5 : 4; age range: 50–82 years) showed both mast cells and neutrophils in the tumor stroma. At ultrathin sections, we identified heterotypic aggregation and intermingling of mast cells and neutrophils. Mast cells had mature phenotype and showed full complement of granules with homogeneous, scroll, particle, and mixed pattern. In addition, we found normal-appearing or early apoptosis showing neutrophils. Conclusion. Our histological findings showed the likely interaction between mast cells and neutrophils in GC. We hypothesize that the granular content of mast cells may be released in small quantity through a mechanism called “kiss-and-run fusion,” which is alternative to well-known massive anaphylactic or piecemeal degranulation.
Highlights
Despite its decreasing incidence and mortality, gastric cancer (GC) still represents the second leading cause of cancer death worldwide [1,2,3]
Neutrophils, mast cells, eosinophils, and dendritic cells may directly infiltrate foveolar epithelium, whereas the lamina propria is permeated by mononuclear cells, such as lymphocytes, macrophages, and plasma cells [6,7,8,9,10]
We report morphological interaction between mast cells and neutrophils in the stroma of human GC
Summary
Despite its decreasing incidence and mortality, gastric cancer (GC) still represents the second leading cause of cancer death worldwide [1,2,3]. 20% of cancer deaths worldwide are associated with unresolved infection or chronic inflammation; prolonged inflammation can lead to mucosal atrophy, which in some patients precedes neoplastic development [4]. Unresolved inflammation may create a microenvironment facilitating cellular transformation and chronic tissue damage. It may trigger repair response including growth and survival factors, tissueremodeling enzymes, and immune regulatory cytokines [5]. The role of immune cell populations in gastric cancerogenesis has not been yet fully clarified [4]. Neutrophils, mast cells, eosinophils, and dendritic cells may directly infiltrate foveolar epithelium, whereas the lamina propria is permeated by mononuclear cells, such as lymphocytes, macrophages, and plasma cells [6,7,8,9,10]
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