Intravenous Immunoglobulin (IVIg) Induce a Protective Phenotype in Microglia Preventing Neuronal Cell Death in Ischaemic Stroke
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Intravenous Immunoglobulin (IVIg) Induce a Protective Phenotype in Microglia Preventing Neuronal Cell Death in Ischaemic Stroke. / Häußler, Vivien; Daehn, Tristan; Rissiek, Björn; Roth, Vanessa; Gerloff, Christian; Arumugam, Thiruma V; Magnus, Tim; Gelderblom, Mathias.
in: NEUROMOL MED, Jahrgang 22, Nr. 1, 03.2020, S. 121-132.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Intravenous Immunoglobulin (IVIg) Induce a Protective Phenotype in Microglia Preventing Neuronal Cell Death in Ischaemic Stroke
AU - Häußler, Vivien
AU - Daehn, Tristan
AU - Rissiek, Björn
AU - Roth, Vanessa
AU - Gerloff, Christian
AU - Arumugam, Thiruma V
AU - Magnus, Tim
AU - Gelderblom, Mathias
PY - 2020/3
Y1 - 2020/3
N2 - Targeting the immune system and thereby modulating the inflammatory response in ischemic stroke has shown promising therapeutic potential in various preclinical trials. Among those, intravenous immunoglobulins (IVIg) have moved into the focus of attention. In a murine model of experimental stroke, we explored the therapeutic potential of IVIg on the neurological outcome and the inflammatory response. Further, we used an in vitro system to assess effects of IVIg-stimulated microglia on neuronal survival. Treatment with IVIg resulted in decreased lesion sizes, without significant effects on the infiltration and activation pattern of peripheral immune cells. However, in microglia IVIg induced a switch towards an upregulation of protective polarization markers, and the ablation of microglia led to the loss of neuroprotective IVIg effects. Functionally, IVIg stimulated microglia ameliorated neuronal cell death elicited by oxygen and glucose deprivation in vitro. Notably, application of IVIg in vivo led to a comparable decrease of apoptotic neurons in the penumbra area. Although neuroprotective effects of IVIg in vivo and in vitro have been established in previous studies, we were able to show for the first time, that IVIg modulates the polarization of microglia during the pathogenesis of stroke.
AB - Targeting the immune system and thereby modulating the inflammatory response in ischemic stroke has shown promising therapeutic potential in various preclinical trials. Among those, intravenous immunoglobulins (IVIg) have moved into the focus of attention. In a murine model of experimental stroke, we explored the therapeutic potential of IVIg on the neurological outcome and the inflammatory response. Further, we used an in vitro system to assess effects of IVIg-stimulated microglia on neuronal survival. Treatment with IVIg resulted in decreased lesion sizes, without significant effects on the infiltration and activation pattern of peripheral immune cells. However, in microglia IVIg induced a switch towards an upregulation of protective polarization markers, and the ablation of microglia led to the loss of neuroprotective IVIg effects. Functionally, IVIg stimulated microglia ameliorated neuronal cell death elicited by oxygen and glucose deprivation in vitro. Notably, application of IVIg in vivo led to a comparable decrease of apoptotic neurons in the penumbra area. Although neuroprotective effects of IVIg in vivo and in vitro have been established in previous studies, we were able to show for the first time, that IVIg modulates the polarization of microglia during the pathogenesis of stroke.
U2 - 10.1007/s12017-019-08571-5
DO - 10.1007/s12017-019-08571-5
M3 - SCORING: Journal article
C2 - 31559534
VL - 22
SP - 121
EP - 132
JO - NEUROMOL MED
JF - NEUROMOL MED
SN - 1535-1084
IS - 1
ER -
