Pathogenicity of Helicobacter ganmani infection in Helicobacter susceptible and resistant mice

Abstract

[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] Helicobacter species are one of the most prevalent bacterial contaminants of laboratory rodents. It is currently unknown whether Helicobacter ganmani, which was first isolated in 2001 from the intestines of laboratory mice, causes significant intestinal inflammatory changes in mice. The goal of this study was to evaluate whether infection with H. ganmani would cause clinical signs or intestional inflammation in mice that are known to be susceptible or resistant to another murine helicobacter, H. hepaticus. Mice were infected with H. ganmani, H. hepaticus, or brucella broth (negative control). Cecal tissue was collected from all mice 4 or 90 days after infection to microscopically score levels of inflammation and to determine changes in expression of inflammatory genes. When compared with negative controls, inflammatory changes in cecal tissue were not significantly greater in H. ganmani infected mice. Analysis of cecal gene expression also showed that H. ganmani infection failed to cause significant elevations of the proinflammatory cytokine interferon-gamma. However, in immunodeficient mice, H. ganmani infection was associated with a significant increase in expression of the pro-inflammatory cytokine IL-12/23p40. Although in this study H. ganmani infection failed to induce cecal inflammation that is the hallmark of H. hepaticus infection, infection was associated with alterations in inflammatory cytokines in immunodeficient mice.