Characterization of ileal dendritic cell distribution in a rat model of acute and chronic inflammation

Authors

  • Manuel A. Silva MD, MSc,

    Corresponding author
    1. Intestinal Disease Research Programme, Department of Pathology and Molecular Medicine, McMaster University, Ontario, Canada
    • Intestinal Disease Research Programme, Department of Pathology and Molecular Medicine, McMaster University, Health Science Centre 3N5C, 1200 Main St W, Hamilton, Ontario, L8N 3Z5, Canada
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  • Mónica Porras,

    1. Cell Biology, Physiology and Immunology Department, Universitat Autònoma, Barcelona, Cataluña, Spain
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  • Jennifer Jury,

    1. Intestinal Disease Research Programme, Department of Pathology and Molecular Medicine, McMaster University, Ontario, Canada
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  • Patri Vergara,

    1. Cell Biology, Physiology and Immunology Department, Universitat Autònoma, Barcelona, Cataluña, Spain
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  • Mary H. Perdue PhD

    1. Intestinal Disease Research Programme, Department of Pathology and Molecular Medicine, McMaster University, Ontario, Canada
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Abstract

We examined ileal dendritic cell (DC) subpopulations in a rat model of indomethacin-induced enteritis to determine changes in phenotype and distribution associated with increased mucosal permeability during acute and chronic stages of inflammation. Sprague-Dawley rats were treated with indomethacin (7.5 mg/kg subcutaneously, 2 injections 48 h apart). Animals were killed at day 4 (acute stage) or at day 15 or 30 (chronic stages); control rats were injected with saline. DC distribution was evaluated by immunohistochemistry for CD103, CD11b, CD83, and CD163; inflammation was assessed by light microscopy; and permeability was determined by flux of horseradish peroxidase in Ussing chambers. In controls, both immature DC subpopulations, CD103+CD11b+CD163CD83 and CD103+CD11bCD163CD83, were observed in the lamina propria, and the CD11b population also was present in Peyer's patches. In acute inflammation, permeability was increased (P < 0.01), and inflamed areas with or without ulcers were observed. CD103+ and CD11b+ (CD83) DCs were absent from inflamed areas, reduced in noninflamed tissues, but present in Peyer's patches. In the chronic stage at day 15, CD103+ and CD11b+ cells were located in inflamed and noninflamed areas and in Peyer's patches. In addition, CD83+ DCs were detected in inflamed areas. At day 30, when we observed a complete microscopic resolution of inflammation, numbers of CD103+ and CD11b+ DCs were increased, and there were CD83+ DCs beneath the epithelial cell layer. We conclude that antigen uptake in acute inflammation may activate resident immature DCs, inducing their migration to lymphoid tissue where they mature and then return to the intestine to play a role in the local inflammatory response.

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