NDLI: Total parenteral nutrition-associated lamina propria inflammation in mice is mediated by a MyD88-dependent mechanism.

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Total parenteral nutrition-associated lamina propria inflammation in mice is mediated by a MyD88-dependent mechanism.

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Total parenteral nutrition-associated lamina propria inflammation in mice is mediated by a MyD88-dependent mechanism.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Feng, Yongjia Teitelbaum, Daniel H. Miyasaka, Eiichi A. Poroyko, Valeriy Gillilland, Merritt G. Mason, Katie L. Falkowski, Nicole R. Erb-Downward, John Huffnagle, Gary B.
Description	Country affiliation: United States Author Affiliation: Miyasaka EA ( Section of Pediatric Surgery, Department of Surgery, University of Michigan, Ann Arbor, MI 48109, USA.)
Abstract	Enteral nutrient deprivation via total parenteral nutrition (TPN) administration leads to local mucosal inflammatory responses, but the underlying mechanisms are unknown. Wild-type (WT) and MyD88(-/-) mice underwent jugular vein cannulation. One group received TPN without chow, and controls received standard chow. After 7 d, we harvested intestinal mucosally associated bacteria and isolated small-bowel lamina propria (LP) cells. Bacterial populations were analyzed using 454 pyrosequencing. LP cells were analyzed using quantitative PCR and multicolor flow cytometry. WT, control mucosally associated microbiota were Firmicutes-dominant, whereas WT TPN mice were Proteobacteria-domiant. Similar changes were observed in MyD88(-/-) mice with TPN administration. UniFrac analysis showed divergent small bowel and colonic bacterial communities in controls, merging toward similar microbiota (but distinct from controls) with TPN. The percentage of LP T regulatory cells significantly decreased with TPN in WT mice. F4/80(+)CD11b(+)CD11c(dull/-) macrophage-derived proinflammatory cytokines significantly increased with TPN. These proinflammatory immunologic changes were significantly abrogated in MyD88(-/-) TPN mice. Thus, TPN administration is associated with significant expansion of Proteobacteria within the intestinal microbiota and increased proinflammatory LP cytokines. Additionally, MyD88 signaling blockade abrogated decline in epithelial cell proliferation and epithelial barrier function loss.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1201746
Journal	The Journal of Immunology
Issue Number	12
Volume Number	190
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-06-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Inflammation Pathology Intestinal Mucosa Microbiology Myeloid Differentiation Factor 88 Immunology Parenteral Nutrition, Total Adverse Effects Animals Flow Cytometry Etiology Mice Mice, Inbred C57bl Mice, Knockout Microscopy, Fluorescence Mucous Membrane Polymorphism, Restriction Fragment Length Real-time Polymerase Chain Reaction Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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