J Vet Sci.  2022 May;23(3):e41. 10.4142/jvs.21274.

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

• Kirthika P
• Park S
• Jawalagatti V
• Lee JH

• KMID: 2530435
• DOI: http://doi.org/10.4142/jvs.21274

Abstract

Background
Proliferative enteritis caused by Lawsonia intracellularis 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 L.intracellularis 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 L. intracellularis.
Results
The mice developed characteristic lesions of the disease and shed L.intracellularis in the feces following oral inoculation with 5 × 10⁷ bacteria. An increase in L. intracellularis 16s rRNA and groEL 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 L. intracellularis infection. Notably, the expression of genes for the vitamin B12 receptor and for secreted and membrane-bound mucins were downregulated in L. intracellularis -infected mice. Furthermore, L. intracellularis 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 L. intracellularis infection and develop potential vaccination and therapeutic strategies to treat PE.

Keyword

Animal model; mouse; mucin; immune response; cytokines