Role of Helicobacter pylori surface structures in bacterial interaction with macrophages.

Abstract

Helicobacter pylori infection is associated with a marked infiltration of the gastric epithelium by neutrophils, macrophages, lymphocytes, and plasma cells. Despite the presence of phagocytes in close vicinty to H pylori microbes a great number of people are unable to eradicate bacteria. To investigate the involvement of multiple bacterial 'adhesins' and some phagocytic receptors in the process of the ingestion of H pylori by macrophages. BACTERIA: H pylori strains differing in the expression of sialic acid dependent (sHA) or sialic acid independent (HA) haemagglutinin and heparan sulphate binding were selected for the study. The uptake of fluorescein labelled H pylori bacteria by a homogenous macrophage cell line J 774A.1 was estimated in a quantitative fluorometric assay. The ingestion of H pylori 17874 and 25 strains expressing sHA was inhibited by the pretreatment of the bacteria with anti-sHA antibodies or fetuin as well as by treatment of the macrophages with neuraminidase. In contrast the uptake of H pylori 17875 strain expressing HA remained unchanged. The phagocytosis of all investigated bacteria was inhibited after the treatment with heparin, hyaluronic acid or vitronectin with fresh but not heat inactivated serum. The results suggest that H pylori surface compounds binding host proteins such as fetuin, heparin/haparan sulphate, hyaluronic acid, and vitronectin in the presence of complement, could allow the bacteria to avoid phagocytosis.