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. 2017 Nov 30;7:16628. doi: 10.1038/s41598-017-16778-4

Figure 5.

Figure 5

HMGB1 induces macrophage activation via the MyD88-TLR2/4 pathway. (A) THP-1 macrophages were co-cultured with particle-treated neutrophils in direct contact in the presence or absence of HMGB1-neutralizing antibodies (HMGB1 Ab). “% extent of activation” represents the extent of activation as indicated by TNF-α release, relative to the full response to particle induction, expressed in percentage (%). Data are shown as means ± SEM for the results of at least three independent experiments. ## p < 0.005, vs. particle-stimulated neutrophils. (B) Partial inhibition of TNF-α production by anti-HMGB1 antibodies was observed for THP-1 cells in a non-contact system and exposed to DNase-digested NETs. Data are shown as means ± SEM and the results of at least three independent experiments. ## p < 0.005, vs. particle-stimulated neutrophils. (C) Neutralizing antibodies targeting TLR2, TLR4, or receptor for advanced glycation end products (RAGE) were added to the co-culture system. Data are shown as means ± SEM and the results of at least three independent experiments. *p < 0.05, vs. resting (control) neutrophils. # p < 0.05, vs. particle-stimulated neutrophils. (D) THP-1 cells with expression of MyD88 (MyD88 KD) or RAGE stably knocked down (RAGE KD) by shRNA were subjected to the direct co-culture system. Data are shown as means ± SEM and the results of at least three independent experiments. *p < 0.05 and **p < 0.005, vs. resting (control) neutrophils. # p < 0.05, vs. particle-stimulated neutrophils.