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. 2017 Jun 30;8:1211. doi: 10.3389/fmicb.2017.01211

FIGURE 2.

FIGURE 2

Pharmacological and genetic inhibition of HDAC1 rescue the 2-AA-mediated immunomodulation. (A) Schematic representation of the 2-AA treatments. The human monocytes THP-1 cells and mouse macrophage RAW264.7 cell cells were left untreated (No Pre: No Tolerization) or pretreated with 2-AA for 24 h or 48 h (2-AA Pre: 2-AA tolerization) respectively, and then stimulated (Sti) with 2-AA. (B) Expression of TNF (1 h) was measured in non-pretreated, 2-AA pretreated and 2-AA + TSA pretreated THP-1 cells following 2-AA stimulation. Transcript levels were assessed by qRT-PCR and normalized to GAPDH. (C) ChIP assay of H3K18ac at the TNF promoter of 2-AA-pretreated, 2-AA and TSA pretreated or non-pretreated THP-1 cells following 3 h 2-AA stimulation, assessed by qRT-PCR with primer covering the promoter site region of TNF relative to GAPDH. (D,E) ELISA of IL-1β and Mcp1 secretion in culture supernatant of 2-AA pretreated vector control RAW264.7 and HDAC1 KD cells following 6 h 2-AA stimulation (n = 3; means ± SDs; p < 0.05, Student’s t-test).