Parenteral Nutrition Induces Organ Specific Alterations in Polymeric Immunoglobulin Receptor Levels

• Published in: The Journal of surgical research 2008-10, Vol.149 (2), p.236-242
• Main Authors: Sano, Yoshifumi, M.D, Gomez, F. Enrique, Ph.D, Hermsen, Joshua L., M.D, Kang, Woodae, M.D., Ph.D, Lan, Jinggang, Ph.D, Maeshima, Yoshinori, M.D, Kudsk, Kenneth A., M.D
• Format: Article
• Language: English
• Subjects: Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Animals; Biological and medical sciences; Emergency and intensive care: metabolism and nutrition disorders. Enteral and parenteral nutrition; General aspects; immunoglobulin A; Intensive care medicine; Intestines - immunology; Male; Medical sciences; Mice; Mice, Inbred ICR; mucosal immunity; parenteral nutrition; Parenteral Nutrition - adverse effects; polymeric immunoglobulin receptor; Random Allocation; Receptors, Polymeric Immunoglobulin - metabolism; Respiratory System - immunology; Surgery
• ISSN: 0022-4804; 1095-8673
• DOI: 10.1016/j.jss.2007.12.790

Background Secretory immunoglobulin A (IgA) prevents pathogen adherence at mucosal surfaces to prevent infection. Polymeric immunoglobulin receptor (pIgR), located on the basolateral surface of mucosal cells, binds dimeric IgA produced by B cells with the cooperation of T cells in the lamina propria. This IgA-pIgR complex is transported apically, where it is exocytosed as secretory IgA to the mucosal surface. Our prior work shows that parenteral nutrition (PN) impairs both airway and small intestine mucosal immunity by reducing T and B cells and IgA levels. This work examines intestinal and respiratory tissue-specific pIgR responses to PN. Methods Cannulated male Institute of Cancer Research mice were randomized to Chow ( n = 10) or PN ( n = 10). After 5 days, animals were sacrificed and lavages obtained from the small intestine, lung (BAL = bronchoalveolar lavage), and nasal airways (NAL). Small intestine, lung, and nasal passage tissues were also collected. Lavage and tissue homogenate IgA levels were quantified by enzyme-linked immunosorbent assay and pIgR by Western blot. Results PN group SIL and NAL IgA levels dropped significantly compared with Chow. PN significantly reduced pIgR levels in the SI while no pIgR change was noted in nasal passages and lung pIgR actually increased with PN. Tissue homogenate IgA levels did not change with PN in the SI while levels in the nasal passage and lung decreased. Conclusions PN impairs airway mucosal immunity by reduction in IgA available for transport rather than via a reduction in pIgR levels. In the small intestine, diminished pIgR is implicated in the deterioration of antibody-mediated mucosal immunity.