Light microscopic and ultrastructural evidence of in vivo phagocytosis of Helicobacter pylori by neutrophils

Helicobacter pylori is believed to cause chronic active gastritis. Infectio n/colonization of the gastric mucosal surface induces a mucosal inflammator y reaction in the form of lymphocytic aggregates, plasma cells and, particu larly. neutrophils, which may, in turn, damage the mucosal epithelium. In v itro studies demonstrate that, in culture, the bacilli are readily phagocyt osed by neutrophils, this evoking a neutrophilic oxidative burst. However, it has been claimed that neutrophils do not phagocytose H. pylori in vivo. In this study of 19 endoscopic biopsies of gastric mucosa with H. pylori-as sociated gastritis, Cresyl violet staining for light microscopy and electro n microscopy are used to demonstrate that, in vivo, neutrophils actively ph agocytose and destroy the bacilli in the epithelial intercellular space and in the mucin on the surface of the mucosa. Direct contact of neutrophils w ith H. pylori was observed in 17 of 17 cases by light microscopy and in 4 o f 15 cases by electron microscopy. Phagocytosis by neutrophils was seen in 14 of 17 cases by light microscopy and in 3 of 15 cases by electron microsc opy. It was most evident in the surface mucus coat where "wolf packs" of ne utrophils were seen attacking the microbes. Ultrastructurally, neutrophil p hagolysosomes contained both intact and partially digested bacteria, convin cing evidence th at the primary function of neutrophils in chronic active g astritis is to destroy H. pylori organisms. This study leaves open the ques tion of whether. or how, neutrophils damage the gastric mucosa.