Morphological and Cellular Features of Innate Immune Reaction in Helicobacter pylori Gastritis: A Brief Review

Abstract

Innate and adaptive immunity are both involved in acute and chronic inflammatory processes. The main cellular players in the innate immune system are macrophages, mast cells, dendritic cells, neutrophils, eosinophils, and natural killer (NK), which offer antigen-independent defense against infection. Helicobacter pylori (H. pylori) infection presents peculiar characteristics in gastric mucosa infrequently occurring in other organs; its gastric colonization determines a causal role in both gastric carcinomas and mucosa-associated lymphoid tissue lymphoma. In contrast, an active role for Epstein-Barr virus (EBV) has been identified only in 9% of gastric carcinomas. The aim of the present review is to discuss the role of cellular morphological effectors in innate immunity during H. pylori infection and gastric carcinogenesis.

Keywords: Helicobacter pylori; eosinophils; gastritis; innate immunity; mast cell; neutrophils.

Figure 1

Gastric bioptic specimens—Ki-67-immunostained cycling epithelial cells in the deep foveolar zone and in the isthmus/neck region; few Ki-67-positive cells are present in deep glandular zone (A, immunoperoxidase, Mayer’s haemalum counterstain, 160×). Epithelial cells of the proliferative zone exhibit enlarged nuclei containing prominent nucleoli (arrows) and cytoplasmic mucin loss (B, haematoxylin and eosin, 400×). (Unpublished personal data).

Figure 2

Intraepithelial mast cell showing partially empty, slightly enlarged, non-fused granules containers, a process similar to piecemeal degranulation; this latter phenomenon may represent a picture related to acute inflammatory reaction during H. pylori infection. (TEM, 8000×—Unpublished personal data).