KMID : 0893420220230030041
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Journal of Veterinary Science 2022 Volume.23 No. 3 p.41 ~ p.41
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Evaluation of host and bacterial gene modulation during Lawsonia intracellularis infection in immunocompetent C57BL/6 mouse model
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Perumalraja Kirthika
Park Sung-Woo Vijayakumar Jawalagatti Lee John-Hwa
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Abstract
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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 ¡¿ l07 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.
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KEYWORD
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Animal model, mouse, mucin, immune response, cytokines
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