Impairment of mucosal immunity by parenteral nutrition: depressed nasotracheal influenza-specific secretory IgA levels and transport in parenterally fed mice
| Autor: | Brock K. King, R. C. Dewitt, Kenneth A. Kudsk, Yong Wu, Kathryn B. Renegar |
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| Rok vydání: | 2001 |
| Předmět: |
Male
Parenteral Nutrition Secretory component Enzyme-Linked Immunosorbent Assay Statistics Nonparametric Mice Immune system Antigen Orthomyxoviridae Infections medicine Animals Immunity Mucosal Interleukin 4 Lamina propria Analysis of Variance biology Lactoferrin business.industry Original Articles Trachea Interleukin 10 Nasal Mucosa medicine.anatomical_structure Immunology Immunoglobulin A Secretory biology.protein Surgery business Respiratory tract |
| Zdroj: | Annals of surgery. 233(1) |
| ISSN: | 0003-4932 |
| Popis: | Our work has implicated diet-induced changes in mucosal defenses as a factor in the increased incidence of pneumonia seen with parenteral feeding. 1,2 These defenses include nonspecific immune defenses such as lactoferrin, peroxidases, defensins, and other inhibitory substances of bacterial growth as well as specific defenses. 3 Specific immunity is primarily due to IgA, which is produced by immune cells within the lamina propria and transported across the mucosal epithelia by secretory component (SC). 4 B and T cells producing and controlling IgA production are sensitized to luminal antigens within the Peyer’s patches of the gut-associated lymphoid tissue (GALT), although an upper respiratory site, the nasal-associated lymphoid tissue, appears active in some animal species. 5 The sensitized cells ultimately home to the lamina propria of both intestinal and extraintestinal sites (e.g., respiratory tract), where they produce antigen-specific IgA. IgA is transported into the mucosal secretions to coat and protect moist mucosal surfaces by neutralizing or otherwise preventing attachment and infection by viruses and bacteria. 5–8 Our work has demonstrated significant defects in specific mucosal immunity during parenteral nutrition (TPN). 9 TPN downregulates the entire system by reducing numbers of both B and T cells within all GALT compartments and lowering secretory IgA levels throughout the mucosal immune system. 9,10 Reduction of the intestinal Th2-type IgA-stimulating cytokines, interleukin 4 (IL-4) and interleukin 10, with intravenous TPN correlates with reduced luminal IgA levels. 11 These changes may explain the increase in intestinal bacterial translocation and the loss of established respiratory antiviral 12 and antibacterial 13 defenses in TPN-fed animals. Although it is tempting to attribute the lowered respiratory and gastrointestinal mucosal secretory IgA levels solely to TPN-induced loss of GALT cell mass, impaired transport by the epithelial cell itself is possible, because parenteral feeding produces mucosal atrophy and changes in cytokine production that could alter epithelial transport function. 14 This study investigates the mucosal transport of intravenously administered polymeric IgA (pIgA) in parenterally fed mice using the selective transport index (STI) and the ability of intravenously administered influenza-specific monoclonal pIgA to reverse TPN-induced impairments in antiinfluenza respiratory mucosal immunity. |
| Databáze: | OpenAIRE |
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