Interaction of Helicobacter pylori (strain 151) and Campylobacter coli with human peripheral polymorphonuclear granulocytes.

Helicobacter pylori associated gastritis is characterized by dense mucosal inflammatory infiltrations with predominantly neutrophilic granulocytes, together with a local and systemic immune response. Nevertheless, the natural course of the infection is chronic in nature, and active phagocytosis of H. pylori by mucosal granulocytes was only rarely observed. The aim of the present study was to investigate with electronmicroscopic methods the interaction of H. pylori with freshly harvested human peripheral granulocytes, with Campylobacter coli as control organism. Bacteria, either untreated or opsonized with complement or antiserum, were coincubated with phagocytes for up to 120 min. After defined time periods the following parameters were electronmicroscopically evaluated: i) internalization of bacteria., ii) morphological characteristics of bacteria and phagocytes, iii) decrease of lysosomes, and iv) by use of myeloperoxidase staining, the characteristics of phagolysosomal fusion. In the absence of complement, both organisms were internalized to a comparable extent. However, in contrast to C. coli, remarkable amounts of H. pylori cells remained extracellularly attached even after 120 min of coincubation, as well as internalized bacteria remained morphologically largely unimpaired. If complement was present, internalization and morphological destruction of H. pylori cells were significantly enhanced. The latter was characterized by rounding and swelling of H. pylori cells. It was already apparent in the extracellular space, and therefore probably induced by a complement effect, rather than by tee phagocytic action. Decrease of lysosomes, in general paralleled the degree of microbial uptake. Myeloperoxidase staining experiments furthermore showed an obviously regular consumption of lysosomal granules. However, if complement opsonization was excluded, lysosomal degranulation was not accompanied by a corresponding degradation of H. pylori cells, the latter indicating an at least partial resistance to phagocyte caused microbicidal mechanisms. In most of those cases ingested H. pylori cells were, in contrast to C. coli, surrounded by a rather "tight" phagosome. A possible explanation for this phenomenon could be a "leakage" of the phagosomal membrane, possibly caused by membranotoxic ammonia produced by the organism. If such an impairment of the phagocytic action would occur in vivo, it could lead to an impaired cellular defense, and therefore contribute to the chronic course of H. pylori infections.