Literature DB >> 20639251

MyD88/TLR9 mediated immunopathology and gut microbiota dynamics in a novel murine model of intestinal graft-versus-host disease.

Markus M Heimesaat1, Axel Nogai, Stefan Bereswill, Rita Plickert, André Fischer, Christoph Loddenkemper, Ulrich Steinhoff, Sandrine Tchaptchet, Eckhard Thiel, Marina A Freudenberg, Ulf B Göbel, Lutz Uharek.   

Abstract

BACKGROUND: The bacterial microflora aggravates graft-versus-host-disease (GvHD) after allogeneic stem cell transplantation, but the underlying mechanisms of manifestations of intestinal GvHD (iGvHD) in the gut remain poorly understood. AIM: To analyse the gut flora composition and the impact of bacterial sensing via Toll-like receptors (TLRs) in iGvHD.
METHODS: By mimicking clinical low-intensity conditioning regimens used in humans, a novel irradiation independent, treosulfan and cyclophosphamide-based murine allogeneic transplantation model was established. A global survey of the intestinal microflora by cultural and molecular methods was performed, the intestinal immunopathology in TLR-deficient recipient mice with iGvHD investigated and finally, the impact of anti-TLR9 treatment on iGvHD development assessed.
RESULTS: The inflammatory responses in iGvHD were accompanied by gut flora shifts towards enterobacteria, enterococci and Bacteroides/Prevotella spp. Analysis of iGvHD in MyD88(-/-), TRIF(-/-), TLR2/4(-/-), and TLR9(-/-) recipient mice showed that bacterial sensing via TLRs was essential for iGvHD development. Acute iGvHD was characterised by increasing numbers of apoptotic cells, proliferating cells, T cells and neutrophils within the colon. These responses were significantly reduced in MyD88(-/-), TLR2/4(-/-), TRIF(-/-) and TLR9(-/-) mice, as compared with wild-type controls. However, TRIF(-/-) and TLR2/4(-/-) mice were not protected from mortality, whereas TLR9(-/-) mice displayed increased survival rates. The important role of TLR9-mediated immunopathology was independently confirmed by significantly reduced macroscopic disease symptoms and colonic apoptosis as well as by reduced T-cell and neutrophil numbers within the colon after treatment with a synthetic inhibitory oligonucleotide.
CONCLUSIONS: These results emphasise the critical role of gut microbiota, innate immunity and TLR9 in iGvHD and highlight anti-TLR9 strategies as novel therapeutic options.

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Year:  2010        PMID: 20639251     DOI: 10.1136/gut.2009.197434

Source DB:  PubMed          Journal:  Gut        ISSN: 0017-5749            Impact factor:   23.059


  119 in total

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2.  Campylobacter jejuni induces extra-intestinal immune responses via Toll-like-receptor-4 signaling in conventional IL-10 deficient mice with chronic colitis.

Authors:  B Otto; L-M Haag; A Fischer; R Plickert; A A Kühl; U B Göbel; M M Heimesaat; S Bereswill
Journal:  Eur J Microbiol Immunol (Bp)       Date:  2012-09-10

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4.  Serum miR-29a Is Upregulated in Acute Graft-versus-Host Disease and Activates Dendritic Cells through TLR Binding.

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Journal:  J Immunol       Date:  2017-02-03       Impact factor: 5.422

5.  Donor TLR9 gene tagSNPs influence susceptibility to aGVHD and CMV reactivation in the allo-HSCT setting without polymorphisms in the TLR4 and NOD2 genes.

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6.  Total abdominal irradiation exposure impairs cognitive function involving miR-34a-5p/BDNF axis.

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Review 7.  Intestinal microbiota-related effects on graft-versus-host disease.

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Review 8.  Acute graft-versus-host disease: a bench-to-bedside update.

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Journal:  Blood       Date:  2014-06-09       Impact factor: 22.113

9.  ST2/MyD88 Deficiency Protects Mice against Acute Graft-versus-Host Disease and Spares Regulatory T Cells.

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10.  Murine Models for the Investigation of Colonization Resistance and Innate Immune Responses in Campylobacter Jejuni Infections.

Authors:  Soraya Mousavi; Stefan Bereswill; Markus M Heimesaat
Journal:  Curr Top Microbiol Immunol       Date:  2021       Impact factor: 4.291

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