Myeloid differentiation primary response gene (MyD) 88 signalling is not essential for intestinal fibrosis development.

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State: Public
Version: Final published version
Serval ID
serval:BIB_86F52D460934
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Myeloid differentiation primary response gene (MyD) 88 signalling is not essential for intestinal fibrosis development.
Journal
Scientific reports
Author(s)
Lutz C., Weder B., Hünerwadel A., Fagagnini S., Lang B., Beerenwinkel N., Rossel J.B., Rogler G., Misselwitz B., Hausmann M.
ISSN
2045-2322 (Electronic)
ISSN-L
2045-2322
Publication state
Published
Issued date
15/12/2017
Peer-reviewed
Oui
Volume
7
Number
1
Pages
17678
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: epublish
Abstract
Dysregulation of the immune response to microbiota is associated with inflammatory bowel disease (IBD), which can trigger intestinal fibrosis. MyD88 is a key component of microbiota signalling but its influence on intestinal fibrosis has not been clarified. Small bowel resections from donor-mice were transplanted subcutaneously into the neck of recipients C57BL/6 B6-MyD88tm1 Aki (MyD88 <sup>-/-</sup> ) and C57BL/6-Tg(UBC-green fluorescence protein (GFP))30Scha/J (GFP-Tg). Grafts were explanted up to 21 days after transplantation. Collagen layer thickness was determined using Sirius Red stained slides. In the mouse model of fibrosis collagen deposition and transforming growth factor-beta 1 (TGF-β1) expression was equal in MyD88 <sup>+/+</sup> and MyD88 <sup>-/-</sup> , indicating that MyD88 was not essential for fibrogenesis. Matrix metalloproteinase (Mmp)9 expression was significantly decreased in grafts transplanted into MyD88 <sup>-/-</sup> recipients compared to MyD88 <sup>+/+</sup> recipients (0.2 ± 0.1 vs. 153.0 ± 23.1, respectively, p < 0.05), similarly recruitment of neutrophils was significantly reduced (16.3 ± 4.5 vs. 25.4 ± 3.1, respectively, p < 0.05). Development of intestinal fibrosis appears to be independent of MyD88 signalling indicating a minor role of bacterial wall compounds in the process which is in contrast to published concepts and theories. Development of fibrosis appears to be uncoupled from acute inflammation.
Keywords
Animals, Collagen/metabolism, Disease Models, Animal, Fibrosis/metabolism, Fibrosis/pathology, Inflammation/metabolism, Inflammation/pathology, Intestinal Mucosa/metabolism, Intestines/pathology, Matrix Metalloproteinase 9/metabolism, Mice, Mice, Inbred C57BL, Myeloid Differentiation Factor 88/metabolism, Neutrophils/metabolism, Neutrophils/pathology, Signal Transduction/physiology, Transforming Growth Factor beta1/metabolism
Pubmed
Web of science
Open Access
Yes
Create date
08/01/2018 17:31
Last modification date
20/08/2019 14:46
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