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. Author manuscript; available in PMC: 2013 Oct 12.
Published in final edited form as: Circ Res. 2012 Aug 17;111(9):1190–1197. doi: 10.1161/CIRCRESAHA.112.277475

Figure 2. Immunomodulation of IL-6 responses to TLR activation in WKY and SHR by prior exposure to nicotine or Ang II.

Figure 2

IL-6 concentrations in supernatants of cultured splenocytes following activation by various TLR ligands: TLR2 (LTA 100 µM), TLR3 (PIC 10 µM), TLR4 (LPS 10 µM), TLR5 (Flag 100 µM), TLR7 (Clo97 1 µM), and TLR9 (CpG 10 µM) are shown in WKY (Panels A and C in black and white) and in SHR (Panels B and D in red). The names of each TLR ligand are shown in Figure 1. Results were obtained after 48 hours in cultures. The effects of 10 µM nicotine (Panels A and B) and of 1 µM Ang II (Panels C and D) are contrasted in WKY and SHR. Bars represent the mean of three separate experiments. Error bars represent standard error of the mean. ***=p<0.001 and **=p<0.01 indicate significantly different responses to TLR alone (open bars) vs. TLR with exposure to either nicotine or Ang II (shaded bars). Of the six TLR ligands tested, nicotine and Ang II altered most significantly the responses to TLR7 and TLR9. Both nicotine and Ang II enhanced dramatically the IL-6 responses to TLR7 and 9 in SHR, whereas nicotine suppressed the response in WKY and Ang II did not alter it significantly. Responses of TNFα and IL-10 were not altered by nicotine or Ang II (data not shown).