Abstract T MP22: Ly6g/c Monocytes Within The Spleen May Be An Important Target For Bone Marrow Mononuclear Cell Therapy In Stroke
Background: We and other investigators have demonstrated that autologous bone marrow mononuclear cells (MNCs) improve stroke recovery in animal models. We assessed whether the spleen, a major homing organ after MNC administration, is a key target organ associated with the benefits of MNCs.
Methods: C57 mice underwent stroke and were treated with autologous bone marrow MNCs or saline IV at 24 hours after stroke. At various time points, spleens were harvested and flow cytometry of the splenocytes was performed (n=4, per group at each time point). In a separate experiment, C57 mice underwent splenectomy two weeks prior to stroke, and then were treated with autologous MNCs IV or saline at 24 hours after stroke (n=10 each group), compared with mice who had intact spleens and were treated with autologous MNCs or saline at 24 hrs after stroke (n=8 to 12 each group). Behavior testes were evaluated up to the 28 days after stroke using corner and ladder rung tests.
Results: Compared to the saline group, MNC treatment did not change the proportion of B cells, CD4 T helper cells, CD8 T cytotoxic cells, Treg cells or NK cells among splenocytes at any time points tested. However, there was an increased proportion of monocytes in MNC treated animals after stroke compared with saline treated animals (p=0.01 at 1 hour, 0.07 at 3hrs, 0.04 at 6 hrs and 0.09 at 24hrs). The Ly6G/C positive cell population among the monocytes were elevated in the MNC group (p=0.01 at 1 hour, 0.09 at 3hrs, 0.08 at 6 hrs and 0.04 at 24hrs). Neural deficits and lesion size were lower in mice without spleens compared to mice with intact spleens. In mice without spleens, MNCs compared with saline had no effect on functional recovery.
Conclusion: Treatment with autologous MNCs may alter specific subpopulations of monocytes in the spleen. The spleen might be a key target organ associated with recovery after treatment with MNCs for stroke.
Author Disclosures: B. Yang: Research Grant; Significant; AHA. P. Kaushik: None. K. Schaar: None. X. Xi: None. J. Aronowski: None. S. Savitz: Research Grant; Significant; NIH.
This research has received full or partial funding support from the American Heart Association, SouthWest - Arkansas, Colorado, New Mexico, Oklahoma, Texas, Wyoming.
- © 2015 by American Heart Association, Inc.