• Arch Surg Chicago · Dec 1997

    A temporal study of TPN-induced changes in gut-associated lymphoid tissue and mucosal immunity.

    • B K King, J Li, and K A Kudsk.
    • Department of Surgery, The University of Tennessee, Memphis, USA.
    • Arch Surg Chicago. 1997 Dec 1; 132 (12): 1303-9.

    BackgroundTotal parenteral nutrition (TPN) is associated with decreases in small-intestinal gut-associated lymphoid tissue (GALT) T cells, B cells, and IgA levels and impairs IgA-mediated defenses in the respiratory tract. The impaired respiratory tract defenses are speculated to be due to reduced respiratory tract IgA levels.ObjectivesTo determine the time course of GALT cell reductions and document any changes in respiratory tract IgA levels in mice receiving TPN.DesignProspective randomized trial.SettingAnimal research laboratory.MaterialsThirty-five male ICR mice weighing 25 to 35 g.InterventionsMice underwent cannulation with intravenous catheters and received chow for 2 days followed by TPN for 0 (n=6), 1 (n=6), 2 (n=6), 3 (n=6), 4 (n=6), or 5 (n=5) days. Mice were killed after receiving TPN their respective number of days. The small intestine was harvested, and washings were obtained from the small intestine and the respiratory tract. Lymphocytes and IgA levels were analyzed by flow cytometry and enzyme-linked immunosorbent assay, respectively.Main Outcome MeasuresLymphocyte yields from Peyer patches, intraepithelial spaces, and the lamina propria; IgA levels from the small intestine and the respiratory tract.ResultsT- and B-cell yields in the Peyer patches and lamina propria were significantly reduced by day 2 (P<.05) and thereafter compared with day 0. The lamina propria CD4+/CD8+ ratio declined significantly by day 4 (P<.05) compared with day 0. Small-intestinal and respiratory tract IgA levels were significantly diminished by day 3 (P<.05) and thereafter compared with day 0.ConclusionTotal parenteral nutrition produces rapid changes in GALT cell profiles and reduces respiratory tract IgA levels consistent with the impairment of respiratory IgA-mediated defenses.

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