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Title: Macrophage dynamics are regulated by local macrophage proliferation and monocyte recruitment in injured pancreas
Authors: Van Gassen, Naomi ×
Van Overmeire, Eva
Leuckx, Gunter
Heremans, Yves
De Groef, Sofie
Elkrim, Yvon
Gysemans, Conny
Stijlemans, Benoît
Van de Casteele, Mark
De Baetselier, Patrick
De Leu, Nico
Heimberg, Harry
Van Ginderachter, Jo A #
Issue Date: May-2015
Publisher: Wiley-VCH
Series Title: European Journal of Immunology vol:45 issue:5 pages:1482-93
Article number: 10.1002/eji.201445013
Abstract: Pancreas injury by partial duct ligation (PDL) activates a healing response, encompassing β-cell neogenesis and proliferation. Macrophages were recently shown to promote β-cell proliferation after PDL, but they remain poorly characterized. We assessed myeloid cell diversity and the factors driving myeloid cell dynamics following acute pancreas injury by PDL. In naive and sham-operated pancreas, the myeloid cell compartment consisted mainly of two distinct tissue-resident macrophage types, designated MHC-II(lo) and MHC-II(hi) macrophages, the latter being predominant. MHC-II(lo) and MHC-II(hi) pancreas macrophages differed at the molecular level, with MHC-II(lo) macrophages being more M2-activated. After PDL, there was an early surge of Ly6C(hi) monocyte infiltration in the pancreas, followed by a transient MHC-II(lo) macrophage peak and ultimately a restoration of the MHC-II(hi) macrophage-dominated steady-state equilibrium. These intricate macrophage dynamics in PDL pancreas depended on monocyte recruitment by CCR2 and M-CSFR as well as on M-CSFR-dependent local macrophage proliferation. Functionally, MHC-II(lo) macrophages were more angiogenic. We further demonstrated that, at least in CCR2-KO mice, tissue macrophages, rather than Ly6C(hi) monocyte-derived macrophages, contributed to β-cell proliferation. Together, our study fully characterizes the macrophage subsets in the pancreas and clarifies the complex dynamics of macrophages after PDL injury. This article is protected by copyright. All rights reserved.
URI: 
ISSN: 0014-2980
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Clinical and Experimental Endocrinology
× corresponding author
# (joint) last author

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