Evaluation of host and bacterial gene modulation during infection in immunocompetent C57BL/6 mouse model.

Background: Proliferative enteritis caused by undermines the economic stability of the swine industry worldwide. The development of cost-effective animal models to study the pathophysiology of the disease will help develop strategies to counter this bacterium.

Objectives: This study focused on establishing a model of gastrointestinal (GI) infection of in C57BL/6 mice to evaluate the disease progression and lesions of proliferative enteropathy (PE) in murine GI tissue.

Methods: We assessed the murine mucosal and cell-mediated immune responses generated in response to inoculation with .

Results: The mice developed characteristic lesions of the disease and shed in the feces following oral inoculation with 5 × l0 bacteria. An increase in 16s rRNA and copies in the intestine of infected mice indicated intestinal dissemination of the bacteria. The C57BL/6 mice appeared capable of modulating humoral and cell-mediated immune responses to infection. Notably, the expression of genes for the vitamin B12 receptor and for secreted and membrane-bound mucins were downregulated in -infected mice. Furthermore, colonization of the mouse intestine was confirmed by the immunohistochemistry and western blot analyses.

Conclusions: This is the first study demonstrating the contributions of bacterial chaperonin and host nutrient genes to PE using an immunocompetent mouse model. This mouse infection model may serve as a platform from which to study infection and develop potential vaccination and therapeutic strategies to treat PE.