Helicobacter pylori infection negatively influences pregnancy outcome in a mouse model.

Abstract

Helicobacter pylori infects the human stomach, causing gastritis, peptic ulcer, and gastric cancer. H. pylori infection has also been related to extra-gastric disorders. We investigated whether H. pylori infection can influence pregnancy in a murine model. Female CD1 mice were infected with the H. pylori SPM326 strain before mating, and then assessed throughout pregnancy for embryo/fetus characteristics and histopathological changes of the endometrium. Infected mice showed higher numbers of resorption and lower fetal weights than noninfected controls. These pathological phenomena were accompanied by macrophage activation, and increases both of CD4+ and CD8+ lymphocytes and of interferon-gamma and major histocompatibility complex class II expression at the endometrial level, as evaluated by immunohistochemistry. During pregnancy, preferential induction of Th2-type cytokines downregulates Th1-type responses, allowing fetal survival. Our results suggest that H. pylori infection can induce activation of resident uterine immune cells and/or recruitment of cells at the endometrial level. It can be hypothesized that the local Th1-type response induced by H. pylori infection could alter the systemic Th1/Th2-type cytokine balance at sites under particular physiopathological conditions of active tissue and/or vascular formation, such as pregnancy. This is the first evidence in an animal model of the possible influence of H. pylori infection on pregnancy. Further work is required on its mechanism and its relevance for humans.