Vascular Alterations in a Murine Model of Acute Graft-Versus-Host Disease Are Associated With Decreased Serum Levels of Adiponectin and an Increased Activity and Vascular Expression of Indoleamine 2,3-Dioxygenase

URN to cite this document:

urn:nbn:de:bvb:355-epub-350566 Copy

DOI to cite this document:

10.5283/epub.35056 Copy

Schmid, Peter M. ; Bouazzaoui, Karin ; Schmid, Karin ; Birner, Christoph ; Schach, Christian ; Maier, Lars ; Holler, Ernst ; Endemann, Dierk H.

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Date of publication of this fulltext: 17 Jan 2017 15:30

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Details

Item type:	Article
Open Access Type:	Gold (with APC)
Journal or Publication Title:	Cell Transplantation
Publisher:	SAGE Publications
Place of Publication:	THOUSAND OAKS
Volume:	2016
Number of Issue or Book Chapter:	25
Page Range:	pp. 2051-2062
Date:	11 November 2016
Institutions:	Medicine > Lehrstuhl für Herz-, Thorax- und herznahe Gefäßchirurgie
Identification Number:	Value Type 10.3727/096368916X691646 DOI
Keywords:	BONE-MARROW-TRANSPLANTATION; STEM-CELL TRANSPLANTATION; NITRIC-OXIDE; INTERFERON-GAMMA; ENDOTHELIAL DYSFUNCTION; IFN-GAMMA; RESISTANCE ARTERIES; MOUSE LUNG; INTERLEUKIN-10; MICE; Vascular graft-versus-host disease (GVHD); Indoleamine 2,3-dioxygenase (IDO); Adiponectin (APN); Cytokines
Dewey Decimal Classification:	600 Technology > 610 Medical sciences Medicine
Status:	Published
Refereed:	Yes, this version has been refereed
Created at the University of Regensburg:	Yes
Item ID:	35056

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Abstract

Graft-versus-host disease (GVHD) is the limiting complication after bone marrow transplantation (BMT), and its pathophysiology seems to be highly influenced by vascular factors. Our study aimed at elucidating possible mechanisms involved in vascular GVHD. For this purpose, we used a fully MHC-mismatched model of BALB/c mice conditioned according to two different intensity protocols with total ...

Abstract

Graft-versus-host disease (GVHD) is the limiting complication after bone marrow transplantation (BMT), and its pathophysiology seems to be highly influenced by vascular factors. Our study aimed at elucidating possible mechanisms involved in vascular GVHD. For this purpose, we used a fully MHC-mismatched model of BALB/c mice conditioned according to two different intensity protocols with total body irradiation and transplantation of allogeneic (C57BL/6) or syngeneic bone marrow cells and splenocytes. Mesenteric resistance arteries were studied in a pressurized myograph. We also quantified the expression of indoleamine 2,3-dioxygenase (IDO), endothelial (eNOS), and inducible NO synthase (iNOS), as well as several pro-and anti-inflammatory cytokines. We measured the serum levels of tryptophan (trp) and kynurenine (kyn), the kyn/trp ratio (KTR) as a marker of IDO activity, and adiponectin (APN). The myographic study showed a correlation of GVHD severity after allogeneic BMT with functional vessel alterations that started with increased vessel stress and ended in eccentric vessel remodeling, increased vessel strain, and endothelial dysfunction. These alterations were accompanied by increasing IDO activity and decreasing APN levels in the serum of allogeneic animals. The mRNA expression showed significantly elevated IDO, decreased eNOS, and elevation of most studied pro-and anti-inflammatory cytokines. Our study provides further data supporting the importance of vessel alterations in GVHD and is the first to show an association of vascular GVHD with hypoadiponectinemia and an increased activity and vascular expression of IDO. Whether there is also a causative involvement of these two factors in the development of GVHD needs to be further investigated.

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