The role of type-specific antibodies in colonization and infection by Helicobacter pylori

Abstract

Helicobacter pylori is a Gram-negative spiral bacterium that colonizes the stomach of humans, causing gastritis, peptic ulcer disease, or gastric cancer. H. pylori infection accounts for a high percentage of mortality and morbidity rates in developing as well as developed countries. H. pylori bacteria reside in the mucus layer covering the gastric epithelium, and therefore the type of protective measures that could confer resistance appear to be limited. Although H. pylori infection stimulates strong local and systemic specific IgA and IgG antibody production, the influence of antibodies on bacterial colonization and gastric inflammation is still controversial. Recent studies in experimental animal models have indicated a non-essential role of specific antibodies for host resistance against H. pylori infection. Recent data show that protection is mediated by T cells, CD4 T helper type 1 cells, in particular. Antibodies are not only dispensable for protection, but they impair both the elimination of bacteria and the development of gastritis. This effect appears to be IgA-dependent and is not a function of specific IgM or IgG antibodies. This review highlights the recent advances in our understanding of how antibodies may influence the development of gastric inflammation and bacterial colonization. Such information can significantly increase our basic knowledge of immune regulation and protection against H. pylori infection, but can also indicate new strategies for vaccine development.