In Vitro and In Vivo Models of Cerebral Ischemia Show Discrepancy in Therapeutic Effects of M2 Macrophages

Virginie Desestret, Adrien Riou, Fabien Chauveau, Tae-Hee Cho, Emilie Devillard, Marilena Marinescu, René Ferrera, Catherine Rey, Marie Chanal, Denis Angoulvant, Jérôme Honnorat, Norbert Nighoghossian, Yves Berthezène, Serge Nataf and Marlène Wiart

PLOS ONE, 2013, vol. 8, issue 6, 1-12

Abstract: The inflammatory response following ischemic stroke is dominated by innate immune cells: resident microglia and blood-derived macrophages. The ambivalent role of these cells in stroke outcome might be explained in part by the acquisition of distinct functional phenotypes: classically (M1) and alternatively activated (M2) macrophages. To shed light on the crosstalk between hypoxic neurons and macrophages, an in vitro model was set up in which bone marrow-derived macrophages were co-cultured with hippocampal slices subjected to oxygen and glucose deprivation. The results showed that macrophages provided potent protection against neuron cell loss through a paracrine mechanism, and that they expressed M2-type alternative polarization. These findings raised the possibility of using bone marrow-derived M2 macrophages in cellular therapy for stroke. Therefore, 2 million M2 macrophages (or vehicle) were intravenously administered during the subacute stage of ischemia (D4) in a model of transient middle cerebral artery occlusion. Functional neuroscores and magnetic resonance imaging endpoints (infarct volumes, blood-brain barrier integrity, phagocytic activity assessed by iron oxide uptake) were longitudinally monitored for 2 weeks. This cell-based treatment did not significantly improve any outcome measure compared with vehicle, suggesting that this strategy is not relevant to stroke therapy.

Date: 2013
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Persistent link: https://EconPapers.repec.org/RePEc:plo:pone00:0067063

DOI: 10.1371/journal.pone.0067063

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