NKT Cell–Deficient Mice Harbor an Altered Microbiota That Fuels Intestinal Inflammation during Chemically Induced Colitis
Autor: | Anuradha Surendra, Nichole K. Escalante, Susan J. Robertson, Stephanie Fieve, Qiaochu Lin, David S. Guttman, Dana J. Philpott, Catherine J. Streutker, Cynthia X. Guo, Thierry Mallevaey, Thirumahal Selvanantham |
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Rok vydání: | 2016 |
Předmět: |
0301 basic medicine
Segmented filamentous bacteria Immunology Cell Prevotella Inflammation Biology Lymphocyte Activation Microbiology Proinflammatory cytokine Mice 03 medical and health sciences Th2 Cells 0302 clinical medicine Immune system medicine Animals Immunology and Allergy Colitis Mice Knockout Dextran Sulfate Fecal Microbiota Transplantation medicine.disease Natural killer T cell Phenotype Gastrointestinal Microbiome stomatognathic diseases 030104 developmental biology medicine.anatomical_structure Natural Killer T-Cells medicine.symptom 030215 immunology |
Zdroj: | The Journal of Immunology. 197:4464-4472 |
ISSN: | 1550-6606 0022-1767 |
DOI: | 10.4049/jimmunol.1601410 |
Popis: | NKT cells are unconventional T cells that respond to self and microbe-derived lipid and glycolipid Ags presented by the CD1d molecule. Invariant NKT (iNKT) cells influence immune responses in numerous diseases. Although only a few studies have examined their role during intestinal inflammation, it appears that iNKT cells protect from Th1-mediated inflammation but exacerbate Th2-mediated inflammation. Studies using iNKT cell–deficient mice and chemically induced dextran sodium sulfate (DSS) colitis have led to inconsistent results. In this study, we show that CD1d-deficient mice, which lack all NKT cells, harbor an altered intestinal microbiota that is associated with exacerbated intestinal inflammation at steady-state and following DSS treatment. This altered microbiota, characterized by increased abundance of the bacterial phyla Proteobacteria, Deferribacteres, and TM7, among which the mucin-eating Mucispirillum, as well as members of the genus Prevotella and segmented filamentous bacteria, was transmissible upon fecal transplant, along with the procolitogenic phenotype. Our results also demonstrate that this proinflammatory microbiota influences iNKT cell function upon activation during DSS colitis. Collectively, alterations of the microbiota have a major influence on colitis outcome and therefore have to be accounted for in such experimental settings and in studies focusing on iNKT cells. |
Databáze: | OpenAIRE |
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