The role of mast cells and eosinophils in chronic gastritis

Abstract

The role of mast cells and eosinophils in influencing the pathology of chronic gastritis remains unclear. We attempted to study the relationship between endoscopy and the mast cell and eosinophil infiltrate. We also studied the role of gene polymorphisms, Helicobacter pylori density and the CagA antibody status in influencing the mast cell and eosinophil infiltrate. One hundred and twenty consecutive patients were studied. Endoscopic evaluation was done and 3 antral biopsies were taken from each patient and were assessed for eosinophilic and mast cell infiltration, H. pylori density and the density of the other inflammatory cells as per the revised Sydney system. Cytokine gene polymorphisms (IL-1beta, IL-1RA and TNF-alpha) were done on the DNA extracted from the peripheral blood by PCR-RFLP. ELISA was done on the patients' serum for the anti-CagA antibody titres. Nodularity is strongly associated with the presence and density of eosinophils on biopsy (P < 0.05). Eosinophil density is strongly associated with the density of H. pylori, neutrophils, lymphocytes, plasma cells, atrophy, ulceration, foveolitis and lymphoid follicles. The mast cell density is not associated with any of the other histopathological variables. Gene polymorphisms and the CagA antibody titres have no relationship to the mast cell and eosinophil density. Eighty-one patients showed positive anti-CagA antibody titres but there was no association with the eosinophilic or the mast cell infiltrate. It is likely that eosinophilic infiltration is influenced by the H. pylori density but the CagA protein has no role to play in influencing the grade of the eosinophilic infiltrate in the Indian context. Cytokine gene proinflammatory polymorphisms have no role to play in influencing the eosinophilic or the mast cell response. It is likely that other mediators are involved in the inflammatory cell responses.

Histopathological profile of gastritis in adult patients seen at a referral hospital in Kenya

“…Similar observations have also been reported by several other workers including recent experimental studies [25] . We are of the opinion that the body of knowledge on eosinopils in gastritis has grown sufficiently since the introduction of the Sydney System, and that more attention needs to be given to the utility of quantitative evaluation of eosinophils in gastritis.…”

Effect of the flavonoid quercetin on inflammation and lipid peroxidation induced by Helicobacter pylori in gastric mucosa of guinea pig

“…Previous work has demonstrated a correlation between a high level of eosinophil leukocyte infi ltration and bacterial density in the gastric mucosa of infected humans and guinea pigs. [38][39][40] In our experiment, eosinophil leukocyte infi ltration was independent of bacterial colonization in the pyloric antrum. Although we cannot explain the cause, it is possible that factors not related to the gastric colonization of H. pylori are responsible.…”

A vaccine against Helicobacter pylori: Towards understanding the mechanism of protection

“…Unexpectedly, they found that mast cells were necessary for vaccine-induced, T cell-mediated protection in the murine model of H. felis infection (Velin et al, 2005). Increased mast cell numbers have also been observed in the gastric mucosa of H. pylori-infected patients (Moorchung et al, 2006) but as in the experimental model (Velin et al, 2005), this increase alone was not protective. Protection required CD4 T cells.…”