Granulocyte macrophage colony stimulating factor improves mucosal repair in a mouse model of acute colitis (P278)

Details

Serval ID
serval:BIB_F3642090CFD0
Type
Inproceedings: an article in a conference proceedings.
Publication sub-type
Abstract (Abstract): shot summary in a article that contain essentials elements presented during a scientific conference, lecture or from a poster.
Collection
Publications
Institution
Title
Granulocyte macrophage colony stimulating factor improves mucosal repair in a mouse model of acute colitis (P278)
Title of the conference
4th Congress of the European Crohn's and Colitis Organisation (ECCO)
Author(s)
Bernasconi E, Favre L, Bachmann D, Bouzourene H, Croze E, Velischko S, Parkinson J, Michetti P, Velin D
Address
5-7 February 2009, Hamburg (Germany)
ISBN
1873-9946
Publication state
Published
Issued date
2009
Peer-reviewed
Oui
Volume
3
Series
Journal of Crohn's and Colitis
Pages
S120
Language
english
Abstract
Background and Aims: Granulocyte-macrophage colonystimulating factor (GM-CSF), a cytokine modulating the number and function of innate immune cells, has been shown to provide symptomatic benefit in some patients with Crohn's disease (CD). Since, it becomes widely appreciated that a timely and spatially regulated action of innate immune cells is critical for tissue regeneration, we tested whether GM-CSF therapy may favours intestinal mucosal repair in the acute mouse model of dextran sulfate sodium (DSS)-induced colitis.
Methods: Mice treated with GM-CSF or saline were exposed for 7 days to DSS to induce colitis. On day 5, 7 and 10, mice were subjected to colonoscopy or sacrificed for evaluation of inflammatory reaction and mucosal healing. Results: GM-CSF therapy prevented body weight loss, diarrhea, dampened inflammatory reactions and ameliorated mucosal damages. Mucosal repair improvement in GM-CSF-treated mice was observed from day 7 on both by colonoscopy (ulceration score 1.2}0.3 (GM-CSF-treated) vs 3.1}0.5 (untreated), p = 0.01) and histological analysis (percentage of reepithelialized ulcers 55%}4% (GM-CSF-treated) vs 18%}13% (untreated), p = 0.01). GM-CSF therapy can still improve the colitis when hematopoietic, but not non-hematopoietic cells, are responsive to GM-CSF, as shown in WT→GM-CSFRKO chimeras. Lastly, we observed that GM-CSF-induced promotion of wound healing is associated with a modification of the cellular composition of DSS-induced colonic inflammatory infiltrate, characterized by the reduction of neutrophil numbers and early accumulation of CD11b+Gr1lo myeloid cells.
Conclusion: Our study shows that GM-CSF therapy accelerates the complex program leading to tissue repair during acute colitis and suggests that GM-CSF promotion of mucosal repair might contribute to the symptomatic benefits of GM-CSF therapy observed in some CD patients.
Open Access
Yes
Create date
01/02/2010 13:54
Last modification date
20/08/2019 16:20
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