Publication: De novo expression of the hemoglobin
scavenger receptor CD163 by activated microglia is not
associated with hemorrhages in human brain lesions
Authors
Holfelder, K. ; Schittenhelm, J. ; Trautmann, K. ; Haybaeck, J. ; Meyermann, R. ; Beschorner, R.
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Publisher
Editores F. Hernandez y Juan F. Madrid. Murcia, Universidad de Murcia, Departamento de Biologia Celular e Histologia
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DOI
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info:eu-repo/semantics/article
Description
Abstract
The main function of CD163 (hemoglobin
scavenger receptor) is to bind the hemoglobinhaptoglobin
complex, thereby mediating extravasal
hemolysis. However, CD163 also has an
antiinflammatory function. After CD163-mediated
endocytosis, hemoglobin is catabolized further by
hemeoxygenase 1 (HO-1). Previously, we found
expression of HO-1 to be restricted to microglia/
macrophages at sites of hemorrhages in human traumatic
and ischemic brain lesions. We now investigated if
CD163 expression is also correlated with hemorrhages
in brain lesions. Methods. Autopsy brain tissue from 44
cases with hemorrhagic brain lesions (32 traumatic brain
injuries/TBI, 12 intracerebral bleedings/ICB), 56 nonhemorrhagic
brain lesions (30 ischemias, 26 hypoxias)
and 6 control brains were investigated. The post injury
survival times ranged from a few minutes to 60 months.
Results. In controls, single perivascular monocytes
expressed CD163, but only single CD163+ microglia
were found in 3/6 cases. CD163+ cells in the
parenchyma (activated microglia/macrophages)
increased significantly within 24 hours after trauma and
ischemia and within 1-7 days following ICB or hypoxia.
Overall, significantly lower and higher levels of
parenchymal CD163+ cells occurred in hypoxia and
ischemia, respectively. Perivascular CD163+ cells also
increased significantly in all pathological conditions. In
areas remote from circumscribed brain lesions (TBI,
ICB, ischemia), significant changes were only found in
ICB and ischemia. Conclusions. De novo expression of
CD163 by activated microglia/macrophages and
CD163+ infiltrating monocytes are neither restricted to
nor predominant in hemorrhagic brain lesions. Thus, the
antiinflammatory function of CD163 probably
predominates, both in hemorrhagic and non-hemorrhagic
brain lesions and points to possible immunomodulatory
treatment strategies targeting CD163
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