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. Author manuscript; available in PMC: 2019 Dec 1.
Published in final edited form as: Inflammation. 2018 Dec;41(6):2101–2109. doi: 10.1007/s10753-018-0853-0

Fig. 3. Tubastatin A treatment increased the percentage of innate immune cells and macrophages in spleen in the lethal septic model.

Fig. 3.

Animals were randomly assigned into 3 groups, and given intra-peritoneal vehicle DMSO or Tubastatin A (70 mg/kg) dissolved in DMSO or 1 h after the CLP. The DMSO mice were used as Sham. Animals were sacrificed and spleens were harvested 48 hours after CLP, and homogenized into single cell suspension, blocked with anti-mouse CD16/32, and stained with anti-mouse CD11b FITC, F4/80 Antigen APC, anti-mouse B220 PE-Cy7, Gr-1 PerCP-Cy5.5, or anti-mouse CD3 APC-eFluor® 780. Flow cytometry was employed to study the different cell populations. Representative plots of innate immune cells, macrophages, neutrophils, B lymphocytes, and T lymphocytes are shown on the left side of the panel (CD11b+, CD11b+ F4/80+, CD11b+ Gr-1+, B220+, CD3+). Tubastatin A treatment significantly increased the percentage of innate immune cells and macrophages as compared to the vehicle-treated CLP group. There were no significant differences in innate immune cells, macrophages, neutrophils, B lymphocytes, and T lymphocytes between the Sham and CLP + TubA groups. Data presented as group means ± SEM (n = 7/group). CLP cecal ligation and puncture, DMSO Dimethyl sulfoxide, TubA Tubastatin A, Sham no cecal ligation and puncture, SSC side scatter.