Friday, July 17, 2015
Grand Hall and Gallery, Ground Floor & 1st Floor (Maritim Hotel)
Despite the proven ability of immunization to reduce Helicobacter infection in mouse models, the precise mechanism of protection has remained elusive. In this study, we evaluated the role of inflammatory monocytes in the vaccine-induced reduction of Helicobacter infection. We first showed by using flow cytometry analysis that CD11b+CCR2+Ly6Clow inflammatory monocytes accumulated in the stomach mucosa during the vaccine-induced reduction of Helicobacter infection. To determine whether inflammatory monocytes play a role in the vaccine-induced reduction of Helicobacter infection, these cells were depleted with anti-CCR2 depleting antibodies. Remarkably, depletion of inflammatory monocytes is associated with an impaired vaccine-induced reduction of Helicobacter infection on day 5 post infection. Finally to determine whether inflammatory monocytes have a direct or indirect role, we studied their antimicrobial activities. We observed that inflammatory monocytes produced TNF-α and iNOS, two major antimicrobial factors. Lastly, by using a Helicobacter in vitro killing assay, we showed that inflammatory monocytes kill H. pylori. Collectively, these data show that inflammatory monocytes play a direct role in the immunization-induced reduction of Helicobacter infection from the gastric mucosa.