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  • Effects of the immunostimulant GcMAF in cerebral ischemia

    Final Number:

    Yoshitaka Kurashiki MD; Keiko T. Kitazato PhD; David Kung MD; Kenji Shimada; Kenji Yagi; Yoshiteru Tada; Nobuhisa Matsushita; Manabu Sumiyoshi MD; Junichiro Satomi; Yoshihiro Uto; Shinji Nagahiro MD

    Study Design:
    Laboratory Investigation

    Subject Category:

    Meeting: Congress of Neurological Surgeons 2013 Annual Meeting

    Introduction: Post-ischemic inflammation is an essential step in the evolution of ischemic brain damage, and it is associated with the repair of injured brain tissue. Macrophages are the main inflammatory effector among the various infiltration immune cells from blood. The group-specific component protein-derived macrophage activating factor (GcMAF) is an unique molecule in that it stimulates macrophage phagocytic activity, but does not stimulate the release of possibly harmful cytokines such as TNFa. We hypothesized that treatment with GcMAF in acute ischemic period exacerbates brain damage, while it may facilitate recovery in the late phase. Using cerebral ischemia model, we studied the effects of GcMAF in the early- and late phase of post brain ischemia.

    Methods: Seven-week-old Wistar male rats were subjected to 120-minutes middle cerebral artery occlusion and reperfusion (MCAO-R). The rats then received GcMAF (40ng/kg/day, ip) for either 1 or 3 days just after MCAO-R. At 7-14 days post MCAO-R the other rats received GcMAF. Neurological deficits and infarct size were compared to animals who received vehicle control (VC). Cytokines including IL-4, -10, -17, TNFa; the expressions of T-cells CD4, CD8, CD14, CD25 and of macrophages CD11b, CD68 were analyzed by flow cytometry and immunohistochemical staining.

    Results: Compared to VC, the infarct volumes were significantly larger on day 3 but not on day 1 in the GcMAF treated animals. The neurological deficits improved on day 1 in all groups, but on day 3 the GcMAF group has significantly worse deficits than the VC group. The experiments of the cytokines and cell markers are ongoing.

    Conclusions: Our data suggest that GcMAF exacerbates brain damage in the early phase after ischemia. Studies on the effect of immunostimulant in the later phase of cerebral ischemic injury are also ongoing.

    Patient Care: This research identifies a detrimental mechanism associated with worse outcome in cerebral ischemia. Further research on inflammation in cerebral ischemia may provide new window of therapy in stroke.

    Learning Objectives: By the conclusion of this session, participants should be able to 1) identify that macrophages activation simulated by GcMAF is associated with worse histological and clinical outcome in the acute phase of cerebral ischemia.


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